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biology unit 2
Terms in this set (107)
4 Eukaryotic Supergroups
Excavata, SAR clade, Archaeplastida, Unikonta
the eukaryotic supergroup that contains flagellated single-celled organisms with a feeding groove
Stramenopiles, Alveolates, Rhizarians
the supergroup that includes red algae, green algae, and land plants
includes animals, fungi, and some protists
The Endomembrane system
A network of membranes inside and around a eukaryotic cell, related either through direct physical contact or by the transfer of membranous vesicles.
organelles of the endomembrane system
nuclear envelope, endoplasmic reticulum, golgi apparatus, lysosomes, vacuoles and the plasma membrane.
evolution of the endomembrane system
The nuclear envelope formed from an infolding of membrane that eventually surrounded nucleus
The rest of the infolded membrane gave rise to the rest of the endomembrane system (ER, Golgi, Lysosome, vesicles, etc)
most likely occurred in the archaea-like prokaryotic cell that is the ancestor of all eukaryotic cells
The engulfment of a cyanobacterium by a larger eukaryotic cell that gave rise to the first photosynthetic eukaryotes with chloroplasts.
evolution of mitochondria
endosymbiosis - came into eukarytoic from preeukaryotic surronded anarobic prokaryotic bacteria
mitochondria has 2 membranes
1. prokaryotic cell
2. host eukaroytic cell
- dependent on the host cell to provide proteins for its function and the host cell depends on it to supply the energy
Evolution of chloroplasts
- Engulfment of a photsynthetic prokaryotic
evidence for primary endosymbiosis
lots of morphological stuff - chloroplasts and mitochondria divide by binary fission, have their own chromosomes that are circular, membrane composition is prokaryotic-like, Mitochondria uses prokaryotic-like proteins / enzymes(ATP synthases is similar to the flagellar motor, electron transport chain is found in prokaryotic cells, etc.)
mitochondrial genes are most similar to the alpha -
proteobacteria (like Rickettsia)
plastid genes are similar to the cyanobacteria
plastids are a group of closely related organelles that
are used for photosynthesis in eukaryotic cells,
they are found in plants and a number of
chloroplasts are the specific type of plastid that
performs photosynthesis in plants.
a process in eukaryotic evolution in which a heterotrophic eukaryotic cell engulfed a photosynthetic eukaryotic cell which survived in a symbiotic relationship inside the heterotrophic cell
plastid-containing protists are found scattered throughout the phylogeny of protists
many protists have plastids, while others once had them and lost them (you can see remnants of the plastid in their cells).
Analogous Trait Possibility
Plastids independently evolved multiple times due to different cyanobacteria engulfing events occurring in different eukaryotic lineages
Homologus trait possibility
one primary endosymbiosis event of a cyanobacteria in the common ancestor of all plastid containing eukaryotes with some lineages losing the plastid.
Secondary Endosymbiosis Possibility (Horizontal Transfer)
Secondary endosymbiosis is the theory that there were
secondary engulfment events where a plastid-carrying eukaryotic photosynthetic cell (red or green algae) was taken up by another eukaryotic cell.
one primary endosymbiosis event occurred in an ancestor of the red and green algae and plants (archaeplastida) and then secondary endosymbiosis spread the plastid to other eukaryotic organisms
name means "ancestral or first plastid"
Evidence for secondary endosymbiosis
The number of membranes in plastids outside of the archaeplastida clade is consistent with secondary endosymbiosis (four membranes in plastids in some protists - extra membranes come from the cell membrane of the eukaryotic cell that got eaten and the endosome of the cell that ate it)
nucleomorph - plastids in the chlorarachniophytes (a member of the rhizaria group) still have the remnants of a nucleus. This is called a nucleopmorph - strong evidence that the cell that was engulfed and maintained as a plastid was eukaryotic, not prokaryotic
remnant of eukaryote genome within 3rd membrane
Eukaryotic sexual life cycles in general
In all eukaryotic sexual life cycles you alternate between diploid (two copies of every chromosome) and haploid (one copy of every chromosome) stages meiosis is the process that gets you from diploid to haploidfertilization is the process that gets you from haploid to diploid
"diploid dominant" animal-like life cycle
(multicellular diploid stage and
single celled haploid stage)
"Alternation of Generations" plant-like lifestyle
plant-like life cycle (multicellular haploid stage and multicellular diploid stage)
fungal life cycle haploid dominant
protist life cycle
Protists have examples of all three of these main types
Many protists also have an asexual component of their life cycle
Some protists are only asexual (no sexual phase)
Eukaryotic Supergroup #1 - Excavata
-Controversial grouping of diverse organisms (page 597)
-group held together mostly by similarities in the cytoskeleton in their flagella
-Many protists in this group have an "excavated" feeding groove which gives this group it's name
-Group is sometimes supported by standard molecular phylogenies, but
-Contain a kinetoplast
(kinetoplast is a mass of amplified, highly structured mitochondrial DNA in their mitochondria. The DNA is replicated multiple times and then made into a structure composed of multiple rings that are all linked together (like the Olympic rings or chain mail))
-kinetoplast function is unknown
-potentially a drug target since the Kinetoplast requires an unusual DNA replication process that human cells don't need to do.
a mass of mitochondrial DNA lying close to the nucleus in some flagellate protozoa.
Causes African trypanosomiasis (sleeping sickness)
Transmitted by bites from the tsetse fly
1. Early stage in blood only (first 1-2 years)
"haploid dominant" fungal like-life cycle.
symptoms start mild
low grade fever, aches, swollen lymph glands, etc)
Late stage - trypanosome cells break through the blood
brain barrier (months / years after initial infection)
goes to brain and causes inflammation that screws
up sleep/ wake cycle
Variant Surface Glycoproteins (VSGs)
Trypanosomes coat the surface of their cells with a protein called a variant surface glycoprotein (VSG)
There are 1,000s of different VSGs in the trypanosome genome
A single trypanosome cell will only express one type of VSG at any one time
-The human body mounts an immune response
(antibodies) to the one type of VSG on the surface of the trypanosomes and kills all the cells that express that specific VSG
- trypanosomes frequently change the type of VSG made on their surface so that subsequent generations will have a different VSG on their cells.
-Trypanosomes with a new VSG won't be killed by the antibody specific for the old VSG form and they will grow inside the body.
-Human immune system can't beat this thing without the help of drugs (or at least that is what we've always thought)
Mechanisms of antigenic variation
1. Expression sites
-positions on chromosomes that express a VSG gene
-There are 15 different expression sites scattered throughout the trypanosome genome.
-Each expression sites contains one VSG gene
-One expression site will be actively transcribed and the mRNAs will be translated
-The VSG gene in that expression site will make the surface glycoprotein that covers the surface of the cell
-The other 14 expression sites are all "off" and not being actively transcribed.Changing the VSG (antigenic variation)
-There are ~15 different Expression sites - all 15 have a different VSG gene in them - 14/15 of these expression sites are transcriptionally silent, while 1/15 is transcriptionally active
-One way to change the VSG is to change which one of the 15 Expression sites is being actively transcribed
-This only explains how you can switch between 15 different VSGs - what about the 1,000 of VSG genes we just talked about? (Klaudia's awesome question!)
-There is also a repertoire of ~1,000 VSG genes
on different chromosomes that aren't in expression sites (this is called the VSG repertoire)
-These reserve VSGs can move into the actively expressed expression site by homologous recombination
-All VSG genes have a short sequence of homologous sequence at either end of the VSG end (In other words, all VSGs have the same sequence on their two ends)
-This homologous sequence can cause "homologous recombination" to happen.
-The new VSG gene from the repertoire will move into the Expression site and the old VSG gene will leave the expression site and be put back into the repertoire.
-Homologous recombination can also occur between Expression sites, moving a VSG gene from a transcriptionally inactive expression site into the transcriptionally active Expression site.
-Using these two main processes trypanosomes can continually change the VSGs on their surface and consistently evade our immune system.
-a diverse monophyletic supergroup named for the first letters of its three major clades stramenopiles, alveolates, and rhizariansextremely diverse / controversial group (page 599)
-Not held together with any nice morphologically derived shared characteristic
-Mostly grouped together based on DNA sequence data
-Phylogenetic group is controversial because there aren't any clear morphological derived traits that all members have and not all molecular phylogenies show this as a monophyletic grouping.
-The ancestor of the alveolates and stramenopiles is thought to have gained a plastid by secondary endosymbiosis of a red algae.
-Most stramenopiles are photosynthetic - example: most "seaweed" you are familiar with is the photosynthetic brown algae. These are
photosynthetic because the ancestor gained the plastid by secondary endosymbiosis.
-Some alveolates are photosynthetic (many dinoflagellates are photosynthetic), but many, like the apicomplexans and ciliates, have lost a functional plastid (although they still retain remnants of their plastid) and are not photosynthetic. ***Dinoflagellates, apicocomplexes, ciliates
-Surrounded Armored cellulose plates for protection
-Have two flagella
-One flagella lies in the back and propels the dinoflagellate forward
-Other flagella lies in groove between plates - causes dinoflagellates to spin
-Many are photosynthetic, but some aren't.
-Dinoflagellates cause Red Tides
(Large, sometimes toxic blooms of photosynthetic dinoflagellates (red because their ancestors picked up a red algae by secondary endosymbiosis) Karenia brevis dinoflagellate that causes red ties in Florida
produces the neurotoxin brevotoxin - makes fish sick (can kill them))
3. brevetoxin contaminates shellfish and can cause sickness in humans if we eat the contaminated shellfish (lobsters, etc). It can cause weird neurological symptoms like tingling hands and feet and reversal of hot / cold sensation
Endosymbionts of coral
-Found inside cells corals (an animal).
-dinoflagellate provide nutrients to the coral due to photosynthesis
-Coral Bleaching: expulsion of dinoflagellates out of the cells of the coral, Caused by heightened temperatures (and possibly CO2 levels /
acidification of oceans)
-Extended high temperatures causes the endosymbiotic photosynthetic dinoflagellates to not be harmful (it is thought that the high temperature damages them and makes them non-photosynthetic - at this point they are just parasites)
-The coral will expel the dinoflagellates (it actually eats them because coral is an animal and animals ingests food - I forgot to say this in class today)
-Bleaching can lead to coral death if the coral doesn't pick up new dinoflagellates
major problem since corals are a major part of marine ecosystems (lots of organisms live in coral reefs)
-A type of parasitic protozoan.
-Some apicomplexan cause serious human disease
-plasmodium is a group of apicomplexans that causes the disease malaria in humans
i. A plastid-like organelle that is the remnant of the red algae derived plastid that was in the ancestor of the stramenopiles and alveolates.
ii. The aplicoplast does not perform photosynthesis anymore, it just works with the mitochondria to help metabolism
iii. Apicomplexans are not photosynthetic organisms - they are all parasites that derived nutrients from a host.
The Apical complex
complicated structure on apical side of cell
ii. basically a little drill that is used for burrowing into other cells iii. All apicomplexans are parasites (drilling into cells is a very
"parasity" thing to do)
plasmodium life cycle
-haploid dominant (like a fungus)
alternates between mosquito and humans (host)
mosquito to human:
i. haploid sporozoites (n) - mosquito saliva to human blood to liver
-in the liver- haploid merozites formed, some become dormant hypnozoits (reactivation=reoccurrence)
-merozoites burst out of the liver cells and infect red blood cells
-Inside RBC- merozoites
become ring stage trophozoites,
-Feeding stage Trophozoites eat hemoglobin and will eventually divide asexually to produce more merozoites
-Merozoites will go out and infect other red
-high fevers when merozoites break RBCs
-Ring-stage trophozoites can alternatively develop into male or female haploid gametocytes (n) inside of Red Blood Cells.
-gametocytes can be male (will make sperm) gametocytes can be female (will make the egg)
-When a mosquito bites an infected patient, human RBCs, merozoites and gametocytes enter the mosquito digestive tract
-Red blood cells and merozoites get digested in mosquito stomach
-Gametocytes respond to the lowered temperature by forming mature eggs and sperm in gut of mosquito
-sperm and egg fuse by fertilization to make a diploid
-zygote forms a single celled diploid ookinete that
migrates through the stomach wall of the mosquito
-attaches itself to the outside of the stomach
-ookinete forms into an oocyst on the outside of the insect stomach.
-The oocyst undergoes meiosis to generate more haploid cells.
-These haploid cells divide by mitosis and form multiple haploid sporozoites.
-haploid sporozoites leave the oocyst and migrate from the outside of the stomach up to the salivary gland of the mosquito and we begin all over again.
Malaria disease symptoms
Associated with high fevers due to the response of our immune system to the merozoites in our blood stream. Sometimes these can be cyclical if all the merozoites break out of red blood cells at the same time (which happens in some plasmodia species).
a dangerous complications of malaria that can cause
Infected RBCs build up in capillaries in the brain.
This causes a breakdown of the blood brain barrier and
swelling in the brain occurs.
Swelling in the brain can cause massive damage /death of
can cause blindness, deafness, coma and death.
Ciliates cell structure
Lots and lots of cilia! (hence the name) - use these for feeding and
No longer have a plastid
2. They still retain plastid genes in their chromosomes, so you
can see that their ancestors once had a plastid (remember that the common ancestor of the Stramenopiles and Alveolates picked up a plastid by secondary endosymbiosis of a red algae.
iii. Have two nuclei - macronucleus and micronucleus 1. Macronucleus
somatic nucleus - keeps the organism alive
makes proteins for the cell to live
DNA is fragmented and endoreplicated
Genes are highly expressed (high level of transcription)
passes genetic information to the next generation during
DNA is not fragmented or endoreplicated
Genes are not highly expressed (very low level of
ciliate asexual reproduction
will reproduce asexually when there is plenty of nutrients.
Developed drugs that combat plasmodia in patients
Developed the insecticide DDT that killed the mosquitoes
2. macronucleus and micronuclei both undergo DNA replication and divide to make two mics and two macs (textbook is incorrect on it's description of asexual reproduction))
3. cytokinesis yields two daughter each having a micronucleus and a macronucleus.
ciliate sexual reproduction
Ciliates will reproduce sexually when nutrients levels are low
Process of Sexual reproduction in Ciliates (called Conjugation):
-Two different mating types come together and a mating
-bridge forms between them.
-Meiosis occurs and this creates 4 haploid micronuclei in each cell
-3 of the 4 haploid micronuclei are degraded
-The one remaining micronucleus divides to form two
genetically identical haploid micronuclei in each cell.
-One haploid micronucleus from each mating type cell is transmitted to the other mating type.
-The two micronuclei (each from a different mating type) fuse together to form a diploid micronucleus
-diploid micronucleus goes through 3 rounds of mitosis
-8 diploid micronuclei form
-The old macronucleus degrades
-Four micronuclei stay as micronuclei while the other four become macronuclei
-Two rounds of cytokinesis forms 4 separate cells each having it's own micronucleus and macronucleus
So each mating process will produce 8 offspring cells (4 from one starting cell and 4 from the other starting cell)
-Tetrahymena is a powerful genetic model system for biomedical genetics.
-Two Unique features of macronucleus that made Tetrahymena a great model organism:
-Macronuclear DNA is fragment into little pieces and then replicated multiple times without cell division (endoreplication).
- In contrast, micronuclear DNA is long and unfragmented.
-THERE ARE LOTS OF TELOMERES AND TELOMERASE ENZYMES IN THE MACRONUCLEUS
-macronucleus is transcriptionally active (high level of gene expression)
- while micronucleus is transcriptionally silent (no genes being expressed).
CHROMATIN OF THE MACRONUCLEUS WILL BE IN THE HIGHLY TRANSCRIBED STATE.
problems with linear chromosomes
Problem #1 - linear DNA (broken chromosomes) in our cells are very unstable
linear DNA is either degraded or it gets stuck to other linear pieces of DNA by Non-homologous end joining.
A broken chromosome will stick to other chromosomes or itself, causing translocations (one part of a chromosome sticking onto another part) or weird ring chromosomes.
Problem #2 - The end replication problem
RNA primers are added onto the lagging strand on
the eukaryotic linear chromosomes during DNA
On the very 5' end of a chromosome, once the RNA
primer is removed, there is no available 3' OH for DNA polymerase to use. It can't fill in this little gap at the 5' end
Thus, the 5' ends of telomeres shorten every round of replication.
Over multiple generations the chromosome should shorten and eventually over time the chromosome should disappear.
-Since the DNA of macronucleus is fragmented and endoreplicated, the macronucleus is essentially a "bag of telomeres" - easy to isolate and determine the sequence of a bunch of telomeres.
-Found that all the fragmented and endoreplicated chromosomes have repeats of TTGGGG on their ends (easy to determine sequence of these ends since they were so abundant in the macronucleus)
-Ends of human chromosomes have similar repeats on them (slightly different sequence)
-The importance of these repeats:
-Repeats prevent the loss of genetic information
during replication since they aren't genes that code for proteins (telomeres can become shorter and "information" isn't lost.)
-Telomere binding proteins bind these repeats and stabilize linear DNA
Telomere repeats form into T-loops.
-The longer single stranded end of the
chromosome is the 5' TTGGGG 3' strand
The other, shorter strand is complementary
- 3' AACCCC 5'.
-These two strands can bind together in
multiple places due to repetitive structure of
-The long single-stranded end loops back on
itself and forms hydrogen bonds (base- pairs) with repeats in the middle part of the telomere.
Makes a little loop called a "T-loop" that protects the ends of the chromosome - keeps it from being degraded or "sticking" to other chromosomes
We must have an enzyme that adds onto the ends of our chromosomes or our species would cease to exist due to our chromosomes being reduced to nothing
Scientists knew an enzyme must exist that adds these repeats onto chromosomes, but they didn't know what enzyme did this - this enzyme is now known to be telomerase
telomeres need to be put on the ends of
chromosomes after fragmentation of DNA to
make a macronucleus
they also need to be added on to the ends during
asexual reproduction since linear DNA molecules
shorten every round of replication
must have a lot of the enzyme that puts on
telomeres (and they do!!!) - good place to look for
Discovery of the telomerase enzyme using tetrahymena cell extracts
Step 1 - Develop a method to test for the presence of the telomerase enzyme
-Add a short piece of telomere DNA (synthetic telomere) in a test tube
-Add a tetrahymena cellular extract to the tube (contains all the proteins/enzymes that are inside a tetrahymena cell)
-Add nucleotides and some other stuff
Found that there was an enzyme present
in tetrahymena cellular extracts that could catalyze the addition of nucleotides onto telomeres
-Get a "ladder" of different size telomeres (each rung on the ladder is a piece of DNA exactly 6 nucleotides longer than the rung of DNA below it because
-Telomere repeats are 6 nucleotides long) when you run all the DNA out on a gel by DNA electrophoresis
-This ladder of DNA shows you that the telomerase enzyme is present in the extract
Step 2: Cell fractionation to purify the protein that does this (separate the telomerase protein away from all the other proteins in the cell so that you can study it)
-Split up the cell extract into multiple fractions (can split the cell extract up by differences in protein charge or difference in protein sizes, etc.)
-Saw that Fractions 9-12 had telomerase activity
-These fractions had a protein in them that wasn't present in the other fractions.
-Look for the protein that is in fractions 9- 12, but isn't in any other fractions. This protein is likely to be telomerase
-Purified the telomerase protein and determined the sequence of amino acids - had a polymerase-like domain (as you would expect)
-found that the human genome also codes for a similar enzyme
Role of telomerase RNA
-The fractions that contained the Telomerase enzyme also had a small RNA molecule in them.
-an enzyme that destroys all RNA (called RNase) blocked all telomerase activity - thus, telomerase need RNA to be present in the fraction in order to work.
-Found that the fully active telomerase enzyme is composed of a complex of telomerase protein (Enzyme) and a single RNA.
Experiments to determine the function of the telomerase RNA
Sequence of part of the telomerase RNA is complementary to the sequence of the telomere repeat sequence
-If you change this sequence in the RNA you also change the sequence of the telomere repeat over a few generations of growth
This result strongly suggests that the telomerase RNA serves as the template strand for the telomerase polymerase
Model for telomerase function
-The telomerase RNA serves as the template
strand for telomerase - tells telomerase what sequence to put into the telomere repeat.
-Technically, Telomerase is considered to be a reverse transcriptase since it reads an RNA template and it makes a DNA strand.
-Telomerase binds to the 3' end of one of the strands and builds off this to elongate the telomere.
-Telomerase can rapidly add hundreds of TTGGGG repeats.
Importance: Function of Telomerase in our bodies / cells #1
-Telomerase is highly expressed in the germline
-functions to ensure sperm and egg have long
telomeres in them for the next generation.
-mice that lack the telomerase enzyme are generally
okay until the sixth generation.
( The sixth generation mice are sterile because all of their offspring (generation 7) inherit short telomeres and they die before being born.)
Importance: Function of Telomerase in our bodies / cells #2
Important for stem cell function and tissue maintenance
-Genetic disorder caused by lowered levels of
telomerase activity (caused by mutations either in the gene that codes for the telomerase enzyme or the gene that creates the telomerase RNA)
-All symptoms of this disease are associated with defects in tissue maintenance by stem cells
example 1: anemia due to lack of blood cells (stem cells in bone marrow fail to divide properly)
example 2: alopecia - loss of hair due to the loss of stem cells that are in hair follicles. These stem cells produce the cells that make the keratin that composes hair and the melanin that gives it pigment. Loss of these stem cells causes baldness / premature gray hair.
-Every time a stem cell divides it produces two
-One daughter cell becomes a cell that will be a
"progenitor cell" that will divide a few times and then differentiate into cells the body needs (like white and red blood cell)
-The other daughter cell stays as a stem cell (self renewal) and keeps dividing throughout the life of the organism (hopefully).
-Stem cells are important for replacing damaged tissues (ie. blood stem cells in our bone marrow replace damaged red blood cells)
- stem cells express telomerase to ensure they can keep dividing to replace damaged tissue
Model for telomerase function in our bodies / cells
-germline cells - express high levels of telomerase
and maintain long telomeres
-stem cells - express intermediate levels of
telomerase and telomere length slowly decreases
-non-stem cell somatic cells of our bodies. Do not
express telomerase and telomeres continually get
shorter when they divide.
This should result in a gradual decrease in telomere
length in stem and somatic cells are we get older. - Telomere length is thought to be important for AGING! older=shorter
Division of mammalian cells in culture - the Hayflick limit
-When mammalian tissue is dissected out of the organism and grown in culture (in vitro) the cells will divide a finite # of times and then stop dividing.
-The number of times that a cell will divide was called the Hayflick limit
- limit correlated with the lifespan of the organism (long- lived organisms produced cells that had more cell divisions)
- this limit correlated with telomere length (cells with longer telomeres divided more).
Note: cancerous cells don't have a Hayflick limit. HeLa cells are a cell culture line that derived from cancerous cells from a patient (Henrietta Lacks) back in the 50's. These cells will divide forever because they express telomerase and keep their telomeres long.
short telomeres tells cells to stop dividing (signals cell cycle arrest)
-tumor suppressor genes - function to inhibit cell division and activate cell cycle arrest (or apoptosis)
-Proto-oncogenes - function to inhibit cell cycle arrest and activate cell division. Proto-oncogene = immature cancer causing gene - a gene that could form cancer if it is mutated so that its activity levels are elevated)
-Normally our cells listen for signals that tell them to divide or not.
-If a cell receives a signal to divide proto- oncogenes will be turned on and tumor suppressors will be turned off.
-If a cell is damaged and/or shouldn't divide then tumor suppressors are turned on and proto- oncogenes are turned off.
-This system keeps our cells dividing when they are supposed to and not dividing when they're not supposed to.
-In cancer cells,
proto-oncogene are mutated in such a way
so that there activty is increased (the
mutant form is called an oncogene)
-tumor suppressors are destroyed
-This leads to high rates of cell division
-Short telomeres are thought to activate tumor
suppressors that will stop cell division before the chromosomes are completely depleted of telomere repeats (chromosomes become very unstable once telomeres are gone).
-When telomeres are short - somatic and adult stem cells stop dividing and the organism ages.
- Consistent with this idea, the over-expression of
telomerase in tumor resistant mice is capable of extending lifespan. Note: This had to be done in tumor resistant mice, because of the role that telomerase plays in cancer!
Importance: Telomerase and cancer
-High levels of Telomerase activity are associated with tumors
-In order to be immortal and continue to divide, it is
thought that cancer cells have to turn on expression
of the telomerase enzyme.
-many tumors show a high level of telomerase expression (late stage)
-(most) late stage cancer cells have a mutation in the promoter regions of their telomerase gene. These mutations cause telomerase to be expressed at a high level and allow the cancer cells to be immortal.
Short telomeres are associated with increased risk of cancer
-Study following patients with short, medium and
-Telomere length was measured in patients
-Telomeres were characterized as long, short of
-Followed these individuals for 10 years and
asked which patients developed cancer
-Patients with short telomeres at the beginning of
the experiment had much higher cancer incidence than patients with medium or long telomeres
-Young tumor cells that are on their way to becoming cancerous have defects in the tumor suppressors so that they can't stop dividing properly. Therefore, these cells will keep growing even if their telomeres are gone.
-This leads to cells having very short / nonexistent telomeres on their chromosomes - makes chromosomes unstable
-Chromosomes with short telomeres are unstable and you will get translocations (two chromosome pieces sticking together incorrectly), etc. - will create lots of genetic diversity that by chance could lead to high rates of cell division.
Example of how a translocation of an unstable chromosome could cause cancer - The Philadelphia chromosome
-a translocation between chromosome 9 and 22.
-This translocation creates a mutant version of a
proto-oncogene that normally resides on
-The mutant version of the proto-oncogene has
much higher levels of activity resulting in continued cell division.
-The over-active mutant version of the proto- oncogene causes cancer and is now called an oncogene (onco= cancer, so oncogene = cancer causing gene).
Chromosomes in tumor cells
-Most tumors have strange chromosomes that are
the mixed together pieces of multiple
-This is thought to cause increased expression of
genes that cause high rates of cell division.
Current model for the role of telomerase and telomeres
Young tumors have:
- short telomeres
-mutations in tumor suppressors
-The continual division despite the short
telomeres = unstable chromosomes = weird chromosomes that will cause increased division rates.
older more advanced tumors:
-high rates of cell division
-turn on telomerase enzyme by selecting for
mutations in the telomerase promoter.
-This keeps the telomeres long to allow high rates
of uncontrolled cell divisions.
Chromatin Structure and Histone Acetyltransferases
-The genes in the macronucleus are highly expressed -we can use the macronucleus to study the modifications of chromatin structure that occur to allow high levels of gene expression.
-Chromatin is a complex of genomic DNA wrapped in histones
-histones are proteins that bind DNA. The DNA wraps around histones.
Euchromatin vs. Heterochromatin:
-Chromatin is tightly packed in regions where
genes are not expressed transcription factors can't bind to the DNA in heterochromatin and the genes in this region stay off.
-Chromatin is loosely packed in regions where genes are highly expressed Transcription factors CAN bind the DNA of gene
in euchromatin and the genes can be expressed.
Regulation of Chromatin packing
-Histones proteins have tails on them that stick outside the DNA/histone complex
-these tails are positively charged because the tails
have a large number of lysine amino acids in them.
-The lysines on these tails can be acetylated
-The + charge of lysine is lost when lysines are acetylated (lysines will be neutral charge)
Model for how we think chromatin packing is regulated (simplified)
-when histone tails are acetylated: chromatin is loosely packaged into euchromatin and genes can be expressed (specific transcription factors can bind to regulatory regions)
-when histone tails are not acetylated (deacetylated): chromatin is tightly packaged into heterochromatin and genes are not expressed [you can simplistically think about the +++ charges on lysines binding tightly to the --- charge on the sugar phosphate backbone of DNA.
-The enzyme histone Acetyltransferase (HAT) acetylates histones and activates gene expression.
-The enzyme histone deacetylase (HDAC) takes the acetyl group off of histones and shuts down gene expression
Verifying that this model of chromatin packaging is correct and identifying the enzyme that acetylates histones
Researchers developed a test to detect histone acetyltransferase activity (you don't need to know how this test works) - tetrahymena cell extracts had histone acetyltransferase activity
Fractionate the macronuclear extract and identify the protein that performs this reaction (basically the same general thing that I showed you with telomerase last class)
Identified a protein that was homologous to the yeast GCN5 protein
known to be a protein that activated
it wasn't known HOW exactly GCN5 functioned
to increase gene expression.
The fact that an tetrahymena enzyme with known HAT
activity had a similar sequence as GCN5, strongly suggested that GCN5 activated transcription by acetylating histones and opening up the chromatin
turned out to be true
The control of Histone Acetylation patterns by HATS and HDACs is extremely important to human health
-Example 1 -Loss of histone acetylation has been linked to age- related declines in learning / cognitive functions in mice
-We know that acetylation patterns get "weird" as we age.
-Old mice show altered levels of histone acetylation which correlates with defects in learning.
-restoring histone acetylation with a drug can cause a recovery of cognitive abilities!
-Example 2: Alzheimer's patients have altered histone acetylation patterns of genes in the neurons of their brains.
-Therefore: Drugs that alter Histone acetylation could have large impacts on memory / learning / addiction etc. in humans
Histone acetylation and Telomeres:
-We now know that telomeres and acetylation patterns of telomeres are linked.
-The histones the ends of our chromosomes are deactylated, so genes that are near telomeres are not expressed.
-It is thought that when telomeres get short, these genes come on and they help signal stop of cell division (contributing to aging, but protecting against cancer).
the researcher who identified the first HAT using
Tetrahymena will most likely win the Nobel Prize one
of these days.
he's won all sorts of smaller, but impressive prizes
Super Group #3: Archaeplastida
Name means "ancestral plastid"
1. primary endosymbiosis of a cyanobacteria happened in the ancestor
of the members of this clade
2. all are photosynthetic
-Group contains the green algae (protists) and the land plants
Super Group #4: Unikonta
unikonta means 1 flagella
a. all members of this clade came from an ancestor that had one flagella
b. most species in this class still have at least one type of cell with one flagella (we have a sperm with one flagella)
-contains a protist only clade (amoebozaons), and the opisthokonts (includes the fungus + their closest protistan relatives and the animals + our closest protistan relatives).
-group of protists that all have "lobed" pseudopodia
pseudopodia = "false feet" - projections off the cell
-Pseudopodia were once thought to be a derived trait of a class of organisms known as "amoeba".
-We now know that pseuodopodia have evolved independently multiple times.
-The amoeoba classification was polyphyletic.
However, all the amoebozoans have "lobed shaped"
pseudopodia and are a monophyletic group.
e. The "-zoan" part of the name means animal. They are called this because they are closely related to animals (and fungus)
Example of an amoebozoan: Cellular slime mold - Dictyostelim discoideum
Life cycle of the cellular slime mold - dictyostelium discoideum
i. Feeding Stage
-haploid solitary amoebas will crawl around using their pseudopodia to propel them and eat bacteria by phagocytosis.
-The solitary amoebas can undergo sexual (mating with other amoebas to make a diploid that undergoes meiosis to make more haloid amoebas) or asexual reproduction (dividing to make more genetically identical amoebas).
ii. Aggregation Stage
-If starvation occurs, amoebas come together to form a migrating aggregate (slug).
-cAMP is a starvation signal that is given off by a
starving amoeba that attracts other amoebas to them.
-Multiple single amoeba chemotax (movement toward a chemical) towards the cAMP source and also secrete cAMP, which increases the signal.
-This causes all the individual amoebae to come
together and form an aggregate that eventually
resembles a slug.
-"slug" will migrate a short distance (they move toward light)
-Slug-like aggregate then undergoes culmination,
where it differentiates into a fruiting body with a stalk
-spores are wind dispersed and germinate into solitary amoebas that are in a different region.
-The cells in the stalk will dry up and die.
The less condensed form of eukaryotic chromatin that is available for transcription.
Eukaryotic chromatin that remains highly compacted during interphase and is generally not transcribed.
An enzyme that covalently links acetate groups to substrates, such as amino acid side chains of proteins.
removes acetyl group
flat, sheetlike extensions from the core of growth cones, located between the filopodia
a temporary protrusion of the surface of an amoeboid cell for movement and feeding.
Common Features of fungi
Heterotrophic but do not ingest food
-can't make bio-macromolecules using inorganic carbon (CO2)
-need to eat complex carbon based bio-macromolecules
-Secrete digestive enzymes (hydrolytic) break down complex molecules to simple molecules that can diffuse through the plasma membrane.
-some fungi secrete enzymes can break down plant cell walls and form close associations with plant cells- allows access to the sugars, etc. produced by the plant
Hyphae - (found in multi-cellular fungi only)
-The body of the multicellular fungi are made up of multiple long threads called hyphae.
-Long and thin hyphae are elongated thin filaments of cells, maximizes surface area
Cell walls of hyphae are made of chitin
-modified glucose molecules that form large polysaccharide polymers
-adjacent polymers are held together with hydrogen bonds
-similar to cellulose in plant cell walls.
-cells are not separated by cross-walls
-one continuous cytoplasm with multiple nuclei allows for easy transport of materials around the
-This is probably the ancestral form of the fungus -
allows for good tranport
-However, this can be detrimental if the hyphae is cut
cytoplasm will all leak out.
-cross-walls (septa) separate different cells
-large pores allow flow of material (organelles
nutrients, etc) between cells
-Flow of materials around the mycelium is not as
-efficient as coenocytic hyphage, but the fungus can
isolate any damaged hyphae pretty easily.
-This is probably a more recent adaptation that helps
protect fungus against injury.
Tip directed growth
-hyphae grow preferentially at their tips
this again, maximizes surface area
-Chitin synthase enzyme is preferentially found on the very tips of the growing hyphae
- build new cell wall as the hyphae grow
The part of the fungus responsible for extracellular digestion and absorption of the digested food.interwoven networks of hyphae that make up the "body" of most fungus (plural mycelia)
Specialized hyphae that allow close association of plant and fungal cells
-modified hyphae that penetrate the cell wall of plants and form a close association with the plant cell
-allows the fungus to get easily exchange nutrients/
minerals with plant cells
-Can be parasitic in some cases (fungus sucks out
-Can also be mutualistic - Arbuscular mycororrhizae
-Named because these branched hyphae look like little trees inside the plants cells (Arbu = arbor = tree)
Animal Trapping Hyphae
-some fungus makes specialized hyphae that allow them to get nutrients from animals
-example evil nematode (C. elegans) killing hyphae
fungus makes a trap that will catch nematodes and immobilize them.
-The hyphae will then rapidly grow into the immobilized nematode and kill it.
-Digestive enzymes will digest the nematode and the hyphae will absorb the smaller digested nutrients
-Really sophisticated little buggers
-Fungus secretes chemicals that attract the nematodes to the traps (secrete nematode sex pheromones)
-In addition, the fungus can sense nematode chemicals and will start producing traps if the nematodes are present - it won't make traps if the nematodes aren't around.
Generalized life cycle of fungus
-Sexually reproducing fungus - have both diploid and haploid part of the sexual life cycle
-The major component of the fungus life cycle is haploid.
-asexually reproducing fungi just have the haploid part of the life cycle
-incredibly successful way of dispersing
-produce millions of offspring, most will die, but some will land on a good environment and germinate -fungal spores are prevalent in the air
Many fungus have an Asexual component of their life cycle
-produce specialized hyphae which form a fruiting body that produces asexual spores.
-Spore germinates into hyphae that form into a mycelium (a mesh of interwoven hyphae)
iv. Separation of plasmogamy and karyogamy in the sexual component of fungal life cycles
Occurs between two different mating types
fusion of cytoplasm only
c. Often not immediately followed by Karyogamy (fusion of nuclei).
Prolonged Heterokaryotic phase
-Heterokaryotic = Hyphae the have two or more genetically different nuclei enclosed within the same hyphae
-Often a long time goes by before fusion of nuclei - --remain Heterokaryotic for a long time (sometimes years)
-Karyogamy- Fusion of nuclei from different mating types. get a diploid nucleus (or multiple diploid nuclei)
-Meiosis quickly follows karyogamy to produce 4 haploid sexual spores (or more if there is an extra round of mitosis after meiosis)
-sister group to the fungi.
-Protists that feed on algae and bacteria - single celled
-Phylogeny suggests that multicellularity is an analogous trait that evolved independently in the animal and fungal lineages (and also plants)
Diversity of Fungi
-most major fungal groups are named for the unique structures they make during sexual reproduction.
-Zygomycetes - zygosporangia
-Ascomycetes - Ascus and Ascocarp
-Basidiomycetes - Basidia and Basidiocarp
Zygomycetes (pages 660-661)
Derived trait is the sexual spore producing structure called the zygosporangium -
-Zygosporangium: structure that forms during sexual reproduction in zygomycetes, a very resistant structure that can survive desiccation, cold,
-The Heterokaryotic stage (has multiple haploid nuclei of the different mating types inside it) Can stay in this form for a long time
-When conditions improve
a. karyogamy occurs - haploid nuclei from opposite mating types fuse
b. produce multiple diploid nuclei inside the zygosporangium with immediately goes into meiosis to make haploid spores.
Glomeromycetes (page 661)
don't have a sexual reproductive structure they all share
Nearly all of them form arbuscular mycorrhizae
1. Mycorrhizae are a mutualistic interaction between plants and
-fungus lives on the roots of the plants and increases mineral absorption for the plant.
plant provides glucose from photosynthesis.
arbuscular Mycorrhizae penetrate through the cell wall of root cells using their arbuscules (these are often called endomycorrhizae. You saw them in lab last week)
D. Ascomycetes - the sac fungus (pages 661-662)
Many very important fungus are in this group - we will talk about many of these fungus.
-Derived trait is the production of sexual spores (ascospores) inside a sac called an ascus
-Many also produce a large fruiting body called an ascocarp.
-This group makes mushrooms (basidiocarp)
-The basidiocarp sexual fruiting body that they form during sexual reproduction.
mixture of two organisms - fungus and photosynthetic algae
-able to adhere to exposed rocks
-break down the rock to gain minerals
-Hyphae are also good at collecting / holding water
b. Algaei. undergoes photosynthesis to provide sugars to the lichen
-algae and fungus can reproduce independently
-algae and fungus can also reproduce as a functional unit when little pieces (called soredia) of the lichen break off and are wind dispersed.
-Lichen are important for ecological succession
when new rock is exposed (volcano, earthquake) nothing besides lichen can grow on it.
-Lichen are very ruggged little creatures that can live on exposed rock and break down the minerals.
-This eventually creates soil that other plants can start growing on.
-In a couple hundred thousand years, the exposed rock will become a lush forest.
fungus break down dead materials (animals / trees)
Very important for recycling of nutrients in ecosystems
Parasites: As we will see some fungus can form parasitic relationships with both plants and animals
Mutualists: fungi can also form
Important mutualists with plants
i. Mycorrhizae (pages 654-655)
myc = fungus and rhiz = roots. So mycorrhizae means "root
Fungal hyphae that form over the roots of plants
a. b. c.
-hyphae can invade into the plant cells of the roots ---form closely associations with the cells of the roots material is easily exchanged between the fungus and plant.
-plant provides nutrients (sugar) for the fungus
-Mutualistic relationship (mostly)
-the fungi provides increased absorption of minerals and water from the soil for the roots
-Most plants grow much better when they have mycorrhizae on their roots.
-This symbiotic association can sometimes be mutualistic (helps both fungus and plants) commensalistic (helps fungus, but doesn't really effect the plants), or parasitic (helps fungus but is harmful to the plant) depending on the exact conditions
-High levels of phosphorous in the soil = fungus is a commensalists (plant growth isn't altered by the presence of the the Mycorrhizae). Soil is rich in minerals, don't need the Mycorrhizae to help you absorb minerals.
-Low levels of phosphorous in the soil = mutualists (plants grow better if they have mycorrhizae because the Mycorrhizae help them absorb the phosphorous)
endo = inside and phyte = plants. So endophyte means "inside
-fungi that live inside plant leaves (and other tissues).
-fungi protect plants against pathogens by producing antibiotic chemicals.
-Plant provide the fungus with nutrients (sugar)
-Most plants are thought to have some type of fungal endophytes living inside their tissues.
-experiments show that plants with endophytes can fight pathogen infections more effectively than plants withoutendophytes
Important mutualists with Animals
Animal / fungus mutualistic relationships are not as common as plant / fungal mutualism but there are some examples.
Example: leaf cutter ants
1. Ants cut leaves and bring them back to their nest
They keep a fungus in their nest (they are the world's first "farmers")
Ants feed the leaves to the fungus and the fungus breaks down the cellulose in the leaves and produces sugars / proteins that the ants can eat
Fungus also detoxifies the leaves (plants are usually full of toxic chemicals to help prevent herbivory)
The ants and fungus are completely reliant on each other - both die without the other
Source of antibiotic chemicals
left a plate of bacteria open on his bench
A fungal penicillium spore landed on the plate and started growing
-The penicillium fungus secreted penicillin which killed the bacteria.
-Scientists were able to isolate penicillin out of the fungus,mass produce it and save millions of lives.
Saccharomyces cerevisiae - the brewer's yeast
yeast gets energy from Fermentation - produces ethanol
and CO2 (and ATP)
Yeast is a seriously awesome genetic model organism -
Awesome power of yeast genetics - Gene knockout technology
a. Importance - in order to determine what a gene does it is useful to examine what goes wrong when that gene is no longer present (stupid house analogy)
The Sir2 gene
Sir2 mutants have a 50% reduction in lifespan
compared to wildtype
Sir2 overexpression increases lifespan substantially
Note: the exact Mechanism of how Sir2 works is not yet completely clear (in reality this has turned out to be a pretty controversial gene, it's exact role in controlling aging is still unclear and is actively being researched).
Aging is also controlled by caloric restriction
Reduce caloric intake = longer lifespan
This was initially discovered in mice. Mice fed low calorie diets in the lab lived longer
Later found that this was also true in yeast, worms, flies, mice (basically every organism in which it has been tested)
Can use yeast to figure out which genes control caloric restriction lifespan extension
Requirement of sir2 for caloric restriction induced lifespan extension.
caloric restriction does not increase the lifespan of sir2 knockout yeast
Suggests that sir2 is part of the genetic pathways that control the response to caloric restriction
Simple starting model: caloric restriction activates SIR2 and high levels of SIR2 activity causes increased lifespan.
Role of the TOR kinase in mediating caloric restriction
The TOR (Target Of Rapamycin) kinase was discovered by the fact that TOR mutants had different responses to rapamycin.yeast mutants with elevated levels of TOR
activity showed decreased sensitivity to rapamycin
normal / wild type yeast are killed by rapamycin
yeast with higher levels of TOR are not killed by rapamycin
this is how the TOR gene got it's name (Target Of Rapamycin)
We now know that rapamycin functions to inhibit TOR. TOR is a kinase that is necessary for cell division and cell growth.
If TOR is shut off by rapamycin, the yeast cells can't grow and divide and they all die.
Rapamycin was found to have potent anti-fungal properties and the company tried to develop it as a drug for treating athlete's foot.ater discovered to be a potent immunosuppressant (we now know that it inhibits cell division of white blood cells in response to an infection)
When the cell is well fed
TOR kinase is active - TOR is activated either directly through the detection of nutrient levels or through insulin signaling (insulin is an animal hormone that
enters the bloodstream in response to food intake)
Active TOR turns on (activates) processes associated with cell growth and division (high levels of protein synthesis)
Active TOR turns off (inhibits) processes associated with starvation
Activity of cellular stress response genes - helps the cell deal with suboptimal conditions (high heat, high oxidation, low nutrient levels)
autophagy - self eating - sending parts of the cytoplasm of the cell to the lysosome for recycling.
When the cell is starving
the TOR kinase is inactivated
Processes associated with cell growth and division will decrease (TOR is not around to keep them on) - protein synthesis levels fall
Processes associated with starvation will
Cellular stress response genes are
These processes have been shown to
decrease aging and increase lifespan.
Possible Model - TOR inhibits SIR2
High nutrient levels - active TOR might
function to inhibit SIR2 activity, which then
causes a lifespan decreases
Starved cell - inactive TOR allows SIR2
activity to increase and the lifespan
Testing this possible model
i. knockout both SIR2 and TOR1ii. Observe that knocking out TOR1 was
able to increase lifespan even if SIR2
was knocked out.
current model (simplified)
Calorically restricted cell [low nutrients]
SIR2 levels are high and TOR activity is
both lead to increased lifespan.
Well-Fed cell [high nutrient levels]i. SIR2 levels are low and TOR activity is
highii. both these things lead to shortened
mouse SIRT1 and telomeres
The SIRT1 gene is one of many genes in mammals that is homologous to SIR2.
SIRT1 overexpression (higher levels of SIRT1 activity) is correlated with longer telomeres
SIRT1 mutant cells (lower / no SIRT1 activity) have shorter telomeres
Function of SIR2 in telomere silencing
SIR2 is a Histonce Deactylase (HDAC) that will
remove acetyl groups from histones at the ends of
Therefore, the ends of chromosomes are silenced
(no gene expression because the histones aren't
It is thought when our telomeres get short,
telomere silencing is disrupted and the genes at the
ends of our chromsomes are expressed.
Expression of the genes at the ends of our
chromosomes is thought to cause aging (stop cell
Therefore, yeast SIR2 and the human SIR2 homologous
genes might be important for controlling telomere
silencing / telomere length
FINAL MODEL (super simplified and only partially understood)
i. Calorically restricted cell (low nutrients 1. SIR2 is activated
SIR2 activation leads to longer telomeres somehow and increased telomere silencing
longer telomeres and telomere silencing lead to life span extension
2. TOR is inhibited
TOR inhibition leads to increased levels of
stress response proteins and autophagy
Stress response proteins and autophagy extend
Well fed cell (high calories)
SIR2 is inhibiteda. telomeres are shortened and telomere
silencing is disruptedb. shorter / non-silenced telomeres lead to a
TOR is activated
a. increased TOR activity inhibits autophagy and stress response
b. no stress response or autophagy leads to decreased lifespan.
Rapamycin functions to increase lifespan by inhibiting TOR, even in high calorie conditions
PArisites of plants
Chestnut Blight a fungal parasite of the American chestnut tree - came to North
America back in the early 20th centurey from trees imported
has decimated American chestnut population
hyphae grow into bark - break through plant cells and get
nutrients from the cells until tree dies
Parasites of plants that also harm us
many fungal parasites of plants secrete mycotoxins that can make us sick. That is why you don't want to eat moldy bread. Evolution has pre- programmed you to "know" that molds are dangerous.
can grow inside peanut shells (and grains that we eat)
produce aflatoxins - a cancer causing mycotoxin
this is why you are advised to refrigerate organic peanut butter.
Refigeration prevents aspergillus growth (non-organic peanut
butter has anti-fungal chemicals in it)
Claviceps purpurea and ergotism
causes the human disease ergotism
fungus gets into a grain of wheat or rye - grain is transformed
into a big brown, fungal infected grain (these infected grains are called ergots)
c. doesn't really harm the plant much, but if ingested by humans causes ergotism
The Claviceps purpurea Funugs in the ergots create tons of chemicals, some of which are toxic / harmful to us (mycotoxins)
lysergic acid is a major compound found in ergots
the raw material for LSD
Causes altered neurological function
Other chemicals will induce vasoconstriction (constriction of the blood vessels)
Parasites of Animals
less common than plant parasites
most animal immune systems can beat fungal infections pretty efficiently
often found only in immuno-compromised individuals (although some fungus can infect healthy animals as well).
Mycosis - fungal infections of animals
Most animal immune systems are really good at beating fungus
so fungal infections in animals are relatively rare
they do occur in immunocompromised people like
patients with AIDS.
Some fungus is able to infect even people with healthy
Example 1: we can get fungal infections of our respiratory tract
(lungs) - aspergillus infection in the lung of a bird (nasty picture
which I thought you might appreciate)
Example 2 - Skin mycoses
i. fungal infection of the skin ii. Example: Ringworm
people used to think this was caused by worms
actually a fungal infection
3. hyphae radiate out from center - causing a ring of infected skin tissue to appear (the ring is the tip of the growing hyphae).
Example 3 - pseudogymnoascus destrucans and white nose syndrome in batsi. ii. iii.
Fungus infects noses and wings of bats and makes their nose appear whiteHyphae penetrate epidermis of hibernating bats and utilizes resources (sugars) in the blood
Map of infection spread
initially observed in 2006 in Howe cavern near us (probably introduced by a German tourist - German bats are not as susceptible to the fungus)
has since spread rapidly throughout the northeast (and beyond)
which causes premature wake from hibernation (wake up in the middle of winter) and eventual death due to no insects being present.It is possible that fungus irritates the bats during hibernation, waking them up and making them use up their energy reserves during grooming
Also possible, that the fungus directly "eats" the
estimated to have killed >6 million (or more) bats.
3.Leads to a loss of fat storageenergy reserves of the bat - still not 100% clear Example 4: Candida auris
Candida is the fungus that causes yeast infections in humans (Candida grows as a yeast). Candida usually responds well to anti-fungal treatments.Candida auris is a super scary, multidrug resistant form of Candida.
First showed up in 2009 in the ear canal of a patient in Japan who had an ear infection.Since then it has spread rapidly across the globe and has been discovered in US hospitals starting in 2015/2016. Only infects immune-compromised individuals, but if a patient becomes infected lethality is very very high (~40%)
This is rapidly becoming a major issue for hospitals in this country
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