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Terms in this set (107)

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)
-Transcriptional switching
-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!)
-Homologous recombination
-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.
-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
blood cells
-high fevers when merozoites break RBCs
-Ring-stage trophozoites can alternatively develop into male or female haploid gametocytes (n) inside of Red Blood Cells.

human-mosquito:
-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
-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.
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
-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,
starvation, etc.
-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
-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.
-Basidiomycetes
-This group makes mushrooms (basidiocarp)
-The basidiocarp sexual fruiting body that they form during sexual reproduction.
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
immune systes
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
d.
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.
iv.
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
1.
2.
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)
1.
2.
3.
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