Lecture 1 Flashcards
(27 cards)
1
Q
cell’s DNA
A
- prokaryote single long DNA molecule
- eukaryote several DNA molecules
- humans body cells 46 chromosomes (23 x 2)
- human gamete 23 chromosomes
- not dividing, DNA is long thing chromatin fibre
2
Q
duplication
A
- two sister chromatids
- attached by adhesive proteins
- as condense, region connect shrinks to narrow area of centromere
- then chromatids pull apart to form chromosomes
3
Q
mitosis
A
- formation of daughter nuclei
- cytokinesis
4
Q
meiosis
A
- non identical daughter cell
- half of the chromosomes
5
Q
phases of mitosis
A
- mitotic (M) : alternated with interphase, mitosis and cytokinesis
- interphase (I) : cell grows, produces proteins and cytplasmic organelles, copies of chromosomes
- first gap interphase, synthesis interphase, second gap interphase (chromosomes only duplicate in S phase)
- interphase (I) :chromosomes duplicate not condensed, nuclear membrane bounds the nucleus
- prophase (P) : chromosomes tightly coiled, sister chromosomes join,
- prometaphase (P) :
- metaphase (M) :
- Anaphase (A) :
- Telphase (T) :
6
Q
Mitotic Phase (M)
A
- alternates with interphase
- includes mitosis and cytokinesis
7
Q
Interphase (I)
A
- 90% of cell cycle
- cell grows by producing proteins and cytoplasmic organelles
- copies chromosomes
- prepares for cell division
- G1 Phase (first gap); S phase (synthesis); G2 Phase (second gap) : cells grow by proteins and for eg. mitochondria and ER, chromosomes duplicated in S phase
- single centrosome replicates forming two centrosomes
8
Q
Late interphate
A
- chromosomes duplicated but not condensed
- nuclear membrane bounds nucleus
- controsome replicated (two centrosomes)
- each centrosomes has two centrioles (animals cells)
9
Q
Prophase (P)
A
- nucleoli disappear
- mitotic spindle forms (centrosomes and mictrotubules extend to form)
- radial arrays of shorter mictorubules for centrosomes called asters
- centrosomes move away from each other (propelled by lengthening microtubules)
10
Q
Prometaphase
A
- nuclear envelope fragments, microtubules for spindle interact with condensed centromere
- kinetochore microtubules for each pole
- nonkinetochore microtubules interact with opposited ends of spindle
- spindle fibers push sister chromatids until arranged at metaphase plate
- kinetochore (proteins and chromosomal DNA at centromere, joined sister chromatids facing opposite directions)
11
Q
Anaphase (A)
A
- centromeres divide (separating sister chromatids)
- pulled to each pole by spindle fibers
- each pole has equivalent collections of chromosomes
12
Q
Telophase (T)
A
- daughter nuclei begin to forms
- nuclear envelopes arise from fragements of parent cell’s nuclear envelope and portions of endomembrane system
- chromosome becomes less tightly coiled
13
Q
Cytokinesis
A
- division of cytoplasm (late telophase)
- formation of cleavage furrow (pinching cell in two)
- vesicles from Golgi apparatus produce cell plate in middle of cell (plants)
14
Q
Mitotic spindle
A
- distributes chromosomes to daughter cells
- composed of microtubules and proteins
- as spindle assembles, elements come for partial disassembly of cytoskeleton
- fibers elongates by more subunits of protein (tubulin)
- starts at centrosomes (nonmemranous organells organising cell’s microtubules)
- centrosome has pair of centrioles; not necessary for division (animals)
15
Q
Kinetochore/nonkinetochore
A
- motor proteins on kinetochore ‘walk’ attached chromosome along microtubule to pole
- excess microtubule sections depolymerise at kinetochore ends
- lengthen cell along axis
- interdigitate and overlap across metaphase plate
- suring anaphase overl reduced by motor proteins attached to microtubules walk using ATP
- as microtubules push apart, lengthen by adding new tubulin monomers at overlapping ends
16
Q
cytokinesis
A
- division of cytoplasm
- cleavage (cleavage furrow forms)
- contractile ring of actin microfilaments associated with molecules of motor protein mysoin (contraction causes pinch)
- [animals]
- during telophase vesicles form Golgi coalesce at metaphase plate (forming cell plate)
- plate enlarges until membranes fuse with plasma membrane at perimeter
- contents of vesilces for new cell wall
17
Q
Mitosis evolved
A
- prokaryotes reproduce by binary fission
- most bacterial genes located on single bacterial chromosome (consists of circulare DNA molecule with proteins)
- chromosome highly folded and coiled in cell
- binary fission replicates beginning at one point on chromosome (origin of replication)
- as replicates, one origin moves to poles
- cell elongates
- once complete, plasma membrane grows inward (dividing parents cell into two daughter cells)
- movement similar to poleward movement of centromere regions of eukaryotic chromosomes
- bacterial lack visible mitotic spindles and microtubules
- some proteins in binary fission related to eukaryotic proteins, related to eukaryotic tubulin and actin
- as evolved, binary fission arose mitosis
- possible intermediate steps (dinoflagellates: replicated chromo. attached to nuc. envel. ; diatoms: spindle develops in nuc.)
18
Q
control system
A
- normal growth
- development
- maintenance
19
Q
cytoplasmic signals
A
- driven by specific chemical signals in cytoplasm
- experiment of cell fusion (different phases fused forming single cell with 2 nuclei; suggests chemicals present in S phase nucleus stimulated fused cell; Mphase with G1 induce 2nd cell to ender mitosis)
- cell control system
cyclicallty operating molecules trigger, coordinate events in cell cycle
20
Q
Checkpoint
A
- stop/go signals
- transmitted withing cell by signal tansduction pathways
- built in for animals
- many come from cellular surceillance mechanisms
- indicate key cellular processes done correctly
- also signals from outside cell
- G1, G2, M major checkpoint phases
- G1; restriction point
- go = complete cycle, divide; stop = exit cycle, nondividing state (G0)
- liver cells called back to cell cycle by external cues for growth/injury factors
- specialised nerve/muscle cells never divide
21
Q
Factors
A
- rythmic fluctuations (protein kinases activate/deactivate other proteins by phosphorylating)
- kinases (present in constant amounts, require 2nd protein, cyclin; cyclin level fluctuate cyclically; cyclin dependent kinases, Cdks)
- cyclin levels sharp rise in Interphase, fall during mitosis
- MPF (maturation-promoting factor) triggers cell’s passage past G2 to M phase (promotes mitosis by phosphorlyrating variety of protein kinases; stimulated fragmentation of nuclear envelope by phosphorlyrating proteins of nuclear lamina; triggers breakdown of cyclin dropping levels during mitosis)
22
Q
internal/external cues
A
- M phase checkpoint ensures chromo. properly attached to spindle before anaphase (ensures daughters do not end up with missing chromosomes)
- signal to delay anaphase originates at kinetochores not attached to spindle microtubules (keeps anaphase-promoting complex, APC, inactive; kinetochores attached then APC activates then cyclin brakdown and inactivation of proteinsholding sister chromatids together)
- external factors: eg. lack of essential nutrients out of culture medium = no cell division
23
Q
Growth Factors
A
- proteins released by group of cells (stimulate division)
- platelet-derived growth factors (PDGF) by platelet blood cells bind tyrosine-kinase receprots of fibroblasts (type of connective tissue)
- triggers sognal-transduction pathways allowing for G1 checkpoint)
24
Q
PDGF
A
- fibroblasts in culture with only divide with meduim containing PDGF
- released in vicinity of injury (proliferation of fibroblasts to help heal wound)
25
Density dependent inhibition
- divide until form single layer on inner surface of culture container
- gap created (cells with grow to fill gap)
- high densities, insufficient growth factors/nutrients cell growth limited
26
anchorage dependence
- anchored to substratum (extracellular matrix of tissue)
- control mediated by pathways involving plasma membrane proteins + elements of cytoskeleton
- cancer cells exhibit neither density-dependent inhibition/ anchorage dependence
27
cancer cells
- divide excessively and invide other tissues
- don't stop dividing when growth factors depleted
- eithe rmanufactures GF / has abnormality in signalling pathway/ abnormal cell cycle control system
- infinite supply of nutrients = infinite division
- can be immortal
- evade destruction proliferate to form tumor
- benign tumor cells at originating site
- malignant tumor = invasive to impair functions of organs
- often detach and carried in blood/lymph system to other tissues (start metastasis)
- unusual number of chromosomes, may secrete signal molecules causing blood vessels to grow toward tumor
- treatment include high energy radiation/ chemotherapy toxic drugs
- target actively dividing cells
- interfere with specific cell cycle steps
- eg. Taxol prevents mitotic depolymerisation (prevents proceeding past metaphase)
- side effects affect normal cells