1
Q
chromosomes
A
- building material: chromatin – complex of DNA + proteins
- each consists of one very long, LINEAR DNA molecule associated w/ many proteins
- when not dividing, each chromosome is in the form of a long, thin chromatin fiber; condenses (coils and folds) only after DNA replication
2
Q
sister chromatids
A
- each chromatid contains an identical DNA molecule
- initially attached all along their lengths by protein complexes called COHESINS; this attachment is known as SISTER CHROMATID COHESION
- each sister chromatid has a CENTROMERE, a region containing specific DNA sequences where the chromatid is attached most closely to its sister chromatid (this attachment is mediated by proteins bound to the centromeric DNA sequences)
3
Q
kinetochore
A
- structure of proteins associated w/ specific sections of chormosomal DNA at each centromere
- spindle microtubules attach during prometaphase
4
Q
polar microtubules
A
- microtubules that don’t attach to kinetochores
- elongate
- by metaphase they overlap and interact w/ other nonkinetochore microtubues form the opposite pole
5
Q
cell elongation
A
- nonkinetochore microtubules do it during anaphase
- nonkinetochore microtubules from opposite poles overlap e/o extensively during metaphase; during anaphase, the region of overlap is reduced as motor proteins attached to the microtubues walk them away from one another, using energy from ATP
- as the microtubues push apart from e/o, their spindle poles are pushed apart, elongating the cell
- at the same time, the microtubules lengthen somewhat by the addition of tubulin subunits to their overlapping ends, so the microtubules continue to overlap
6
Q
chromosomal poleward movement
A
- “Pacman” mechanism: motor proteins on the kinetochores “walk” the chromosomes along the microtubules, which depolymerize at their kinetochore ends after the motor proteins have passed
- chromosomes are “reeled in” by motor proteins at the spindle poles; microtubues depolymerize after they pass by these motor proteins
7
Q
cytokinesis
A
begins during anaphase/telphase
8
Q
cell cycle time
A
- interphase: 90 percent
- M phase: <1hr
- S phase: 10-12 h
- G1: 5-6 h (most variable in length in diff cell types)
- G2:4-6 h
- each cell: 1 division in 24 hours
9
Q
cleavage furrow
A
- shallow groove in cell surface near the old metaphase plate
- on the cytoplasmic side is a contractile ring of actin microfilaments associated w/ myosin molecules
- the two proteins interact, causing the ring to contract
- the contraction of the microfilament is like the pulling of a drawstring
10
Q
bacterial proteins
A
- one resembling actin functions in chromosome movement
- one related to tubulin helps pinch plasma membrane inward
11
Q
binary fission
A
- cell grows to 2x its size then divides to form 2 cells
- initiated when the DNA begins to replicate at a specific place on the chromosome called the ORIGIN OF REPLICATION
- soon after, one origin copy moves toward the other end of the cell
- replication finishes, plasma membrane grows inward, new cell wall deposited, 2 daughter cells result
12
Q
cell division: dinoflagellates
A
- chromosomes attach to nuclear envelope, which remains intact during cell division
- microtubules pass thru nucleus inside cytoplasmic tunnels, reinforcing the spatial orientation of the nucleus, which then divides in a process reminiscent of bacterial binary fission
13
Q
cell division: diatoms and some yeasts
A
- nuclear envelope remains intact
- microtubues form spindle within nucleus
- microtubues separate chromosomes; nucleus splits into 2 daughter nuclei
14
Q
G0 phase
A
- G1 checkpt is most impt
- if go-ahead signal isn’t received, cell will exit cycle, switching into nondividing state called G0
- most cells of human body are in G0 phase
15
Q
anaphase
A
- commences suddenly when the cohesins holding together the sister chromatids of each chromosome are cleaved by an enzyme called SEPARASE
- once the chromatids become separate, full-fledged chromosomes, they move toward opposite ends of the cell
16
Q
cell cycle regulatory molecules
A
- protein kinases: give go-ahead signals at G1 and G2
- many of these kinases are actually present at a constant concentration in the growing cell, but much of the time they’re in inactive form; to be active, they must be attached to a CYCLIN, a protein that gets its name from its cyclically fluctuating concentration in the cell
- b/c of this requirement, these kinases are called cyclin-dependent kinases, or Cdks
17
Q
MPF
A
- first cyclin-Cdk complex that was discovered (in frog eggs)
- “maturation-promoting factor” but can be thought of as “M-phase-promoting factor” b/c it triggers the cell’s passage past G2 checkpt into M phase
- when cyclins that accumulate during G2 associate w/ Cdk molecules, the resulting MPF complex phosphorylates a variety of proteins, initiating mitosis
- MPF acts both directly as a kinase and indirectly by activating other kinases
18
Q
MPF activity
A
peaks during M, has fallen abruptly by G1, rises from S to M
19
Q
MPF termination
A
- during anaphase, it switches itself off by initiating a process that leads to destruction of its own cyclin
- the Cdk persists in the cell, inactive until it becomes part of MPF again by associating w/ new cyclin molecules synthesized during the S and G2 phases of the next round of the cycle
20
Q
MPF specific situations
A
- MPF causes phosphorylation of various proteins of the nuclear lamina, which promotes fragmentation of the nuclear envelope during prometaphase of mitosis
- MPF may contribute to molecular events required for chromosome condensation and spindle formation during prophase
21
Q
internal signal ex
A
- occurs at M checkpt
- anaphase doesn’t begin until all the chromosomes are properly attached to the spindle at the metaphase plate; as long as some kinetochores are unattached, the sister chromatids remain together, delaying anaphase
- only when the kinetochores are properly attached to the spindle does the appropriate regulatory protein complex become activated
- once activated, the complex sets off a chain of molecular events that activates SEPARASE, which cleaves the COHESINS, allowing the chromatids to separate
- this mechanism ensures that daughter cells don’t end up w/ missing/extra chromosomes
22
Q
external signals
A
- cells fail to divide is an essential nutrient is lacking in the culture medium
- even if all other conditions are favorable, most types of mammalian cells divide in culture only if the growth medium includes specific growth factors
23
Q
PDGF
A
- platelet-derived growth factor; made by blood cell fragments called platelets
- PDGF required for division of FIBROBLASTS, a type of connective tissue cell
- fibroblasts have PDGF receptors (RTKs) on their plasma membranes; binding of PDGF molecules to these receptors triggers a signal transduction pathway that allows the cells to pass G1 chekpt and divide
24
Q
PDGF stimulation
A
when an injury occurs, plateletts release PDGF in the vicinity. the resulting proliferation of fibroblasts helps heal the wound.
25
density-dependent inhibition
- phenomenon in which crowded cells stop dividing
- cultured cells normally divide until they form a single layer of cells on the inner surface of the culture container; then they stop
- if some cells are removed, those bordering the open space begin dividing again to fill the space
- follow-up studies revealed that the binding of a cell-surface protein to its counterpart on an adjacent cell sends a growth-inhibiting signal to both cells, preventing them from moving forward in the cell cycle even in the presence of growth factors
26
anchorage dependence
- most animal cells exhibit this
| - to divide, they must be attached to a sub-stratum
27
"immortality" of cancer cells
- can go on dividing indefinitely in culture if they're given a continual supply of nutrients
- HeLa cells (from a tumor taken from Henrietta Lacks) have been reproducing in culture since 1951
- normal mammalian cells in culture divide only 20 - 50 times before stopping
28
transformation
- converts normal to cancer cell
- immune system normally recognizes a transformed cell and destroys it; if cell evades destruction, it may proliferate and form a tumor, a mass of abnormal cells w/in otherwise normal tissue
29
benign tumor
the abnormal cells may remain at the original site if they have too few genetic and cellular to survive at another site. don't cause serious problems, can be completely removed w/ surgery
30
malignant tumor
includes cells whose genetic and cellular changes enable them to spread to new tissues and impair the functions of one or more organs.
31
cell surface changes
abnormal changes cause cancer cells to lose attachments to neighboring cells and the ECM, allowing them to spread into nearby tissues.
32
metastasis
- The spread of cancer cells to locations distant from their original site.
- a few tumor cells may separate from original tumor, enter blood and lymph vessels, and travel to other parts of the body
