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Final Exam - New Material

Terms in this set (170)

Why do cells reproduce?

organism growth, replacement of lost or damaged cells, and organism reproduction

What signals cell reproduction?

- extracellular molecules called growth factors (GFs)/mitogens
- GF-receptor triggers signal-transduction relay (results in molecular changes that stimulate (or inhibit) cell reproduction)

many growth factors signal through RTKs to activate the Ras-Map kinase pathway
- mutations in the Ras G protein occur in many types of cancer
- many RTK pathways are involved in growth factor signaling for cell division

main events of cell division

1) duplication of DNA
- chromatin changes, chromosome duplication
2) growth of cell in size
3) segregation of DNA
- chromosomes movement
- nuclear division (in eukaryotes) / binary fission (prokaryotes)
4) cytoplasmic division

types of cellular reproduction

- asexual: binary fission (used by prokaryotes, mitotic division (used by eukaryotes)
- sexual (whole organism reproduction): meiotic division, often used for organism reproduction in eukaryotes

binary fission and mitotic division both result in genetically identical daughter cells

binary fission (prok.): "division in half"

single-celled eukaryotes use mitosis in binary fission (ex: amoeba)

multicellular eukaryotes use mitotic and meiotic division

eukaryotes use mitosis for organism growth (multicellular), organism reproduction (single-celled and some multicellular)
- ex: fragmentation in sea stars, budding in hydra, growth of plant from clipping

single bacterial chromosome = circular DNA molecule

most genes are carried on this

- prokaryotes: binary fission
replication begins at the origin: 2 origins are created and move toward opposite ends of the cell as replication continues

- prokaryotes: binary fission
how chromosomes move and how their positions are established is not fully understood - some proteins similar to eukaryotic actin and tubulin involved

- prokaryotes: binary fission
growth: cell elongates during chromosome replication

differences between prokaryotic and eukaryotic cell division

- nuclear membrane
- genome on multiple chromosomes (euk.)
- growth & DNA replication are separate steps (euk.)
- cytoplasmic division: cytokinesis , still last step (euk.)
- now have a nucleus (euk.)

eukaryotic cell cycle

1) interphase (90%)
- growth (G1, G2)
- DNA Replication (S)
2) mitotic (M) phase
- mitosis: nuclear division/chromosome segregation
- cytokinesis: cytoplasmic division

during 3 interphase phases, the cell grows in size: duplicate organelles, proteins, and DNA (S phase) to prepare for division into 2 cells during M phase

different cell types take a different amounts of time to complete the cell cycle:
- time of cycle varies depending on cell type: skin = very fast, muscle = never
- checkpoints to regulate growth @ each step

G0/non-dividing phase: daughter cells may either exit the cycle (G0) or begin the cycle again

DNA replication, origins of replication, centromere: the cell has to replicate its entire genome
- chromosomes must be duplicated, so that 1 copy of each chromosome can be passed on to the daughter cell
- this copying of the DNA begins at specific places on the chromosome called "origins of replication," just as we saw for the single origin in the bacterial chromosome

prior to replication, the chromosomes are long thin filaments of chromatin, but they become condensed following replication

the result of each eukaryotic DNA replication is the formation of duplicated chromosomes
- each duplicated chromosome contains 2 identical sister chromatids (containing identical DNA material) that are attached all along their lengths by protein complexes (cohesins)
- most close attachment occurs at the "waist" of the condensed chromatid pairs, called the centromere (each chromatid on either side of the centromere is called an "arm")

later in the cell division cycle, these sister chromatids will separate and move to opposite sides of the cell so that each daughter cell will get one
- once they are separated, they are once again considered individual chromosomes

M phase is a continuum of changes, a dynamic process

mitosis:
- prophase
- prometaphase
- metaphase
- anaphase
- telophase
- cytokinesis (usually, but not always, overlaps with telophase)

chromosomes condense, nucleoli disperse, sister chromatid visible attached along entire length, mitotic spindle begins to form, centrosomes start to separate

nuclear membrane breaks down, centrosomes move to poles of cell, microtubules extended from centrosomes capture the sister chromatid pairs by attaching to the kinetochore protein complexes at the centromeres, non-kinetochore microtubules from opposite poles also attach to stabilize the spindle

3 types of microtuble

kinetochore, interpolar/non-kinetochore, astral

2 sets of kinetochore proteins per duplicated chromosomes

one on each sister chromatid, facing in opposite directions, so can be pulled to opposite poles
- each human kinetochore binds 20-40 microtubules, yeast kinetochore binds just as one microtubule

metaphase (longest stage of mitosis)

duplicated chromosomes line up in center/midline of cell
- attached to microtubules from both poles
- eukaryotes have centrioles

- cohesin proteins are cleaved, sister chromatids separate and are pulled along microtubules to opposite ends of the cell, so that each is a full-fledged chromosome
- cell elongates as nonkinetochore microtubules lengthen
- at end, two sides of cell have complete, equivalent collections of chromosomes

chromosomes are not reeled in, but microtubules actually shorten at the kinetochore end
- microtubule growth at plus ends of interpolar microtubules

microtubule motor proteins operate a kinetochore
- linked to microtubule and to kinetochore and use ATP hydrolysis to remove tubulin subunits from the microtubules

spindle poles and two sets of chromosomes move farther apart
- motor protein sliding force interpolar microtubules, moving in opposite directions
- pulling force of motor proteins associated with microtubule motor proteins on astral microtubules that are also associated with the cell cortex

nuclear membrane reforms in each daughter cell, chromosomes decondense, spindle disappears

occurs now that mitosis is complete
- formation of a cleavage furrow by plasma membrane, which pinches cell in two

one major difference between plant and animal cells is that plant cells have a cell wall in addition to a plasma membrane, while animal cells have only a plasma membrane

What step of cell division is most affected by the difference between plant and animal cells' plasma membranes?

cytokinesis must be different in plant cells (cell wall)
- vesicles deliver new cell wall to be laid down

cytokinesis in animal cells is accomplished by constriction of a contractile ring - forms the furrow

accomplished by formation and constriction of a ring made up of actin and myosin
- ring is assembled around the equator of the cell during early anaphase, and as it constricts, it generates the shape changes that we observe (belt-like)

signaling by the anaphase spindle directs cytokinesis - provides spatial and temporal precision
- formation of this actin-myosin contractile ring is directed by the anaphase spindle which is the same structure that aligns and segregates the chromosomes
- at anaphase onset, signals are delivered to the equatorial cortex to promote formation of the ring (the anaphase spindle is also required to promote constriction of the ring as well, since disrupting the spindle at any step will cause cytokinesis to fail

G2 pre-prophase in plants

- preprophase band of microtubules vanishes by prophase but determines orientation of cytokinesis

double cylinder of microtubules mediating plant cytokinesis
- kinesin motors move Golgi vesicles to plus ends of microtubules
- fusion of Golgi vesicles forms cell plate (growing wall sandwiched between two membranes)

phragmoplast expands in diameter so microtubules are lined up with growing edges of cell plate

mitosis on drugs

a number of different drugs can target different parts of mitosis

proteasome inhibitor: metaphase arrest

inhibits RhoA - cytokinesis

inhibits a motor protein that separates the spindle pores

cell cycle has two irreversible points

- replication of genetic material (S)
- separation of the sister chromatids (M)

cell cycle can be put on hold at specific points called checkpoints
- process is checked for accuracy and can be halted if there are errors (temporarily or permanently)
- allows cell to respond to internal and external signals

chemical regulation of the cell cycle involves the presence or absence of specific molecules

the cell cycle pauses at specific points (checkpoints), only proceeding if certain molecules are present

cell cycle regulated at each checkpoint by internal and external signals

- animal cells with built-in STOP signals that battle cell cycle: they must be overridden by go-ahead signals
(cellular surveillance mechanisms involved in the stop)

3 major checkpoints

G1, G2, M phase checkpoints (but also some within S)

G1 checkpoint (restriction point)

pRB binds and inhibits transcription factors involved in G1 progression
- pRB active until phosphorylated down stream of growth factor signaling pathway (p'n turns pRB off so gene transcription can begin
- for many cells, the G1 checkpoint seems to be the most important one
- if a cell receives a go-ahead signal at the G1 checkpoint, it will usually complete the S, G2 and M phases and divide
- if a cell does not receive the go-ahead signal, it will exit the cycle, switching into a nondividing state called the G0 phase

external factors, soluble molecules called "growth factors," promote passage through G1 checkpoint

nerves and muscle always in G0 - most cells in cell body in G0 at any given time

at each checkpoint, the cell asks itself questions to be sure it is ready to proceed

G1: do I have a growth signal? no stop signal like growth /too close to other cells?
S phase: is my DNA completely replicated?
G2: are my chromosomes lined up correctly? am I big enough and replicated?

internal signals

various proteins functioning in the cell cycle must complete their jobs to move from one stage of the cell cycle to the next
- these proteins are regulated by cyclin-dependent kinases (Cdks), which in turn are regulated by cyclins (Cdks depends on this) and by phosphorylation

MPF kinase (cyclin-Cdk)

active only in certain parts of the cell cycle (M)
- these kinases bind to different cyclin proteins in different phases of the cell cycle and the active CDK-cyclin complexes each phosphorylate particular proteins that promote progression through that particular cell cycle phase
- CDKs are found in the cell at all times, but cyclins show rhythmic patterns in their levels throughout the cell cycle

MPF: mitosis promoting factor (kinase)

- accumulation of MPF allows cells to pass through G2 checkpoint and into mitosis
- shuts off when cyclin component is degraded at end of M

cyclin levels are rising in G2 and high in M, whereas other cyclins would be high in other phases of the cell cycle

the cell will not progress past the G2 checkpoint if there are problems
- if the cell is not big enough, DNA not ready (other proteins in the cell regulate this)
- choices are either to pause the cell cycle and fix the problem or to commit suicide to prevent the propagation of the error

p53 protein is a key mediator of the checkpoint to prevent continuation of the cell cycle when there are problems

p53 is mutated in a lot of cancers (TSG) because without p53, no checkpoint control

regulated expression of specific cyclins define each cell cycle phase

external signals:
- chemicals: nutrients, growth factors (ex: injury stimulates release of platelet-derived growth factor (PDGF) from platelets
- physical factors: anchorage dependence, density-dependent inhibition (mediated by cell-cell containing signaling)

What if a problem is detected at the checkpoint?

pause & repair or apoptosis

p53 is normally ubiquinated by Mdm2 and targeted by degradation in the protease
- DNA damage activates kinases, like the Chk2 kinase that phosphorylate p53 and prevent it from being ubiquinated
- it can go on to promoted treatment of genes involved in cell cycle arrest and/or apoptosis

relatively unspecialized cells that can reproduce indefinitely and differentiate into specialized cells of one or more types

potential uses of stem cells:
- replacing damaged tissues
- treating degenerative diseases
- treating genetic diseases

cell differentiation patterns are less well established in embryonic cells and become more established over time

after fertilization in animals, the zygote divides mitotically to create an undifferentiated ball of cells

in the regulation of cleavage divisions, G1 and G2 phases of cell cycle short or eliminated
- in animals, it's controlled by the activity of particular cyclins and Cdks (exert different levels of control over checkpoints in the cycle of mitosis
- end result of cleavage divisions: a hollow ball of cells

a hollow ball of still undifferentiated cells in humans
- compared to blastulas of other organisms

cell determination sets the stage for more obvious cell differentiation

cell determination: molecular decision to become a particular type of cell
- cells become determined prior to differentiation
- takes place in stages over time
- cells become committed by cytoplasmic determinants, cell-cell interactions, and gene activation

induction causes cells to influence the determination of their neighbors

scientists are learning which genes control which events of cell differentiation and morphological development

apoptosis also complement cell growth and gene expression to sculpt body parts

stem cell research helps us learn how cells are programmed

embryonic stem cells (ESC) come from embryos and have different characteristics than adult stem cells
- can develop into almost any cell type, and therefore may have a greater therapeutic potential compared to adult stem cells
- some ethical concern about use and non-use of human embryos

induced pluripotent stem cells (iPS cells)

- adult/differentiated cells reprogrammed to act like embryonic cells
- first performed in 2006 in mouse skin cells
- performed in 2007 in human skin cells
- effectiveness and utility still uncertain and a work in progress

one method of creating embryonic stem cells is to induce adult stem cells to dedifferentiate
- scientists have done just that by inserting either specific genes or proteins into adult cells
- the expression of these genes causes the differentiated to act like pluripotent stem cells

this technology offers the potential to create immune matched stem cells for therapy, just like cloning, except it does not involve destroying an embryo

problems with iPS cells

- viral vector for delivery can integrate into the genome of the cells and cause damage
- c-Myc causes cancer if cells are implanted into a mouse (inactivation of c-Myc following establishment of iPS cells may work)

cancer cells form in our body every day
- all starts with errors in cell reproduction/mitotic cell division

cancer in a nutshell

- mutations within a cancer gene or regulatory regions
- chromosome abnormalities = altered gene expression
- abnormal cell cycle activities lead to increasing damage to genetic material
- variable initiation and progression in each patient

What is the largest risk factor for cancer?

a benign mole can become a malignant tumor

cancers = diseases of unregulated cell reproduction
- if proteins that stimulate cell cycle progression are overactive: too much cell reproduction (proto-oncogenes)

if proteins that inhibit cell cycle progression are inactive, too much cell reproduction (tumor suppressor genes)

if cell cycle goes haywire, have uncontrolled reproduction
- density/anchorage dependent growth, normally stop signals but not for cancer cells

also, normal cells do not live forever, transformation cells are "immortal"
- checkpoints at each step
- chromosomal problems/too fast division: mutations
- knowing cause of cancer

proto-oncogenes

signal cells to progress through the cell cycle at the appropriate time
- mutations in these genes cause them to be overestimated, causing too much cell division

tumor suppressor genes

signal cells to pause the cell cycle to fix mistakes
- mutations in these genes cause them to be under-expressed, allowing damaged cells to divide inappropriately

BRCA1 and BRCA2 are tumor suppressor genes that produce DNA repair proteins
- tumor suppressor genes like p53 produce proteins that can induce apoptosis instead of allowing the cell to progress through the cell cycle

how cancer cells proliferate:

- density-independent "growth" (no contact inhibition)
- anchorage-independent growth
- independence of "growth" factor signals
- telomeres do not indicate when to stop proliferating (no senescence)

HeLa cells are from a cervical tumor: uncontrolled reproduction of cervical cells
- HPV infection: can cause cervical cancer and other cancers of the genital areas

cervical cancer was first proposed to be sexually transmitted more than 100 years ago

a tiny non-living particle that only reproduces inside living cells (not visible under a light microscope)
- a nucleic acid genome
- protein coat
- outer envelope (sometimes)

How do viruses cause cancer?

directly: cause increased/uncontrolled proliferation of infected cells, leading to tumor formation
indirectly: create environment in the infected cell or tissue that makes it more likely that loss of proliferation control will occur
- HIV: increased risk for directly developing cancers caused by KSHU (Kaposi's sarcoma), EBV, HPV, HBU, HCV

How do viruses infect cells?

- lytic, transient infection: kills the host cell and causes an immune response, so it can be cleared
- latent infection (chronic): many viruses that directly cause cancer create latent infections (use cell to make virus proteins but no new virus particles are released, evades immune systems, persist for a long time)

all HPV strains express E6 and E7, but only few (high-risk) strains cause cervical cancer
- E6 and E7 are oncogenic (affect cell cycle)
- E5 regulates gene expression downstream of EFG

cervical cancer is only associated with some high-risk HPV strains
- more than 50% of women will have an HPV infection
- most are temporary, low risk for cancer

few strains of HPV persist as chronic infections
- high risk of cervical cancer
- triggers cervical dysplasia (pap smear detection)

epithelial cells, skin (external body covering), lining of body cavities (internal body coverings)

in tissues that support body (muscle, bone)

leukemias, lymphomas

cancers of blood-forming tissues

tissue are composed of cells and extracellular matrix

in plants, each cell surrounds itself with extracellular matrix in the form of a cell wall, which is made chiefly of cellulose and other polysaccharides

an osmotic swelling pressure on plant cell walls keeps plant tissue turgid

cellulose microfibrils in the plant cell wall confer tensile strength, while other cell-wall polysaccharides resist compression

the orientation in which the cellulose microfibrils are deposited in the cell wall controls the orientation of plant cell growth

animal connective tissues provide mechanical support to organs and limbs; these tissues consist mainly of an extracellular matrix, which is secreted by a sparse scattering of embedded cells

in the extracellular matrix of animals, tensile strength is provided by the fibrous collagen proteins, while glycosaminoglycans (GAGs), covalently linked to proteins to form proteoglycans, act as space-fillers and provide resistance to compression

transmembrane integrin proteins link extracellular matrix proteins such as collagen and fibronectin to the intracellular cytoskeleton of cells that contact the matrix

cells are connected to one another via cell junctions in epithelial sheets that line all external and internal surfaces of the animal body

cell adhesion proteins of the cadherin family span the epithelial cell plasma membrane and bind to identical cadherins in adjacent epithelial cells

at an adherens junction, the cadherins are linked to intracellular actin filaments; at a desmosome junction, they are linked to intracellular keratin intermediate filaments

during development, the actin bundles at the adherens junction that connect cells in an epithelial sheet can contract, helping the epithelium to bend and pinch off, forming an epithelial tube or vesicle

hemidesmosomes attach the basal face of an epithelial cell to the basal lamina, a specialized sheet of extracellular matrix; the attachment is mediated by transmembrane integrin proteins, which are linked to intracellular keratin filaments

tight junctions seal one epithelial cell to the next, barring the diffusion of water-soluble molecules across the epithelium

gap junctions form channels that allow the direct passage of inorganic ions and small, hydrophilic molecules from cell to cell; in plants, plasmodesmata form a different type of channel, which traverses the cell walls, is lined by plasma membrane, and allows both small and large molecules to pass from cell to cell

most tissues in vertebrates are complex mixtures of cell types that are subject to continual turnover

most tissue of an adult animal are maintained and renewed by the same basic cell processes that generated them in the embryo
- as in the embryo, these processes are controlled by intercellular communication, selective cell-cell adhesion, and cell memory

in many tissues, non-dividing, terminally differentiated cells are generated from stem cells, usually via proliferating precursor cells

embryonic stem cells (ES cells) can proliferate indefinitely in culture and remain capable of differentiating into any cell type in the body - that is, they are pluripotent

induced pluripotent stem cells (iPS cells), which resemble ES cells, can be generated from the cells of adult mammalian tissues, including those of human, through the artificial expression of a small set of transcription regulators

pluripotent stem cells can be induced to form specific cell types and even small organs (organoids) in suitable culture conditions, providing powerful models for studying human development and genetic diseases

cancer cells fail to obey the social constraints that normally ensure that cells survive and proliferate only when and where they should, and do not invade regions where they do not belong

cancers arise from the accumulation of many mutations in a single somatic cell lineage; they are genetically unstable, having increased mutation rates and, often, major chromosomal abnormalities

unlike most normal human cells, cancer cells typically express telomerase, enabling them to proliferate indefinitely without losing DNA at their chromosome ends

most human cancer cells harbor mutations in the p53 gene, allowing them to survive and divide even when their DNA is damaged

the mutations that promote cancer can do so either by converting one copy of a proto-oncogene into a hyperactive (or over-expressed) oncogene or by inactivating both copies of a tumor suppressor gene

sequencing of cancer genomes reveals that most cancers have mutations that subvert the same key pathways controlling cell proliferation, cell growth, cell survival, and the response to DNA damage
- in different cases of cancer, these pathways are subverted in different ways

knowing the molecular abnormalities that underlie a particular cancer one can begin to design treatments targeted specifically to those abnormalities

adherens junctions

make an adhesion belt that keeps tissues from separating as they stretch and contract

thin extracellular layer that lies underneath epithelial cells and separates them from other tissues

A calcium-dependent adherence protein, important in the adhesion of cells to other cells.

any malignant growth or tumor caused by abnormal and uncontrolled cell division

structure that connects a cell to another cell or to extracellular matrix

A rigid layer of nonliving material that surrounds the cells of plants and some other organisms.

cellulose microfibril

Long, thin strand of cellulose that helps strengthen plant cell walls

A glycoprotein in the extracellular matrix of animal cells that forms strong fibers, found extensively in connective tissue and bone; the most abundant protein in the animal kingdom.

connective tissue

A body tissue that provides support for the body and connects all of its parts

a type of intercellular junction in animal cells that functions as a rivet, fastening cells together

differentiated cell

a cell that has become specialized to become a specific type of cell (such as a liver or udder cell)

embryonic stem (ES) cell

An undifferentiated cell type derived from the inner cell mass of an early mammalian embryo and capable of differentiating to give rise to any of the specialized cell types in the adult body

layer of skin cells forming the outer and inner surfaces of the body

extracellular matrix

The substance in which animal tissue cells are embedded, consisting of protein and polysaccharides.

a cell in connective tissue that produces collagen and other fibers.

An extracellular glycoprotein secreted by animal cells that helps them attach to the extracellular matrix.

A type of intercellular junction in animals that allows the passage of materials between cells.

genetic instability

An increased rate of mutation often caused by defects in the systems that govern the accurate replication and maintenance of the genome; the resulting mutations sometimes drive the evolution of cancer.

Innermost compartment of the mitochondrion

glycosaminoglycan (GAG)

Polysaccharide chain that can form a gel that acts as a "space filler" in the extracellular matrix of connective tissues; helps animal tissues resist compression.

A type of desmosome in which integrins are the prominent cell adhesion molecules.

induced pluripotent stem (iPS) cell

Somatic cell that has been reprogrammed to resemble and behave like a pluripotent embryonic stem (ES) cell through the artificial introduction of a set of genes encoding particular transcription regulators.

In animal cells, a transmembrane receptor protein with two subunits that interconnects the extracellular matrix and the cytoskeleton.

The spread of cancer cells beyond their original site

a gene that in certain circumstances can transform a cell into a tumor cell.

a growth that is similar to an organ in the body

An open channel in the cell wall of a plant through which strands of cytosol connect from an adjacent cell.

Cells that are capable of developing into most, but not all, of the body's cell types

A glycoprotein containing a protein core with attached long, linear carbohydrate chains.

a gene that regulates normal cell division but that can become a cancer-causing oncogene as a result of mutation or recombination

unspecialized cell that can give rise to one or more types of specialized cells

A type of intercellular junction in animal cells that prevents the leakage of material between cells.

A group of similar cells that perform the same function.

tumor suppressor

A gene that codes for a protein product that inhibits cell proliferation; inactive in cancer cells.

tumor suppressor gene

A gene whose protein products inhibit cell division, thereby preventing uncontrolled cell growth (cancer).

Member of a family of extracellular signal molecules that regulates cell proliferation and migration during embryonic development and that maintains stem cells in a proliferative state

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