Term
| why would it be necessary to go retrograde |
|
Definition
RER proteins that contain the amino acid sequence KDEL (lys, asp,glu,leu) should stay in RER
Some RER enzymes accidentally “escape” to Golgi in COPII vesicles
These enzymes can be retrieved by KDEL receptors in COPI vesicles and returned to RER |
|
|
Term
| what is the role of lysosomes |
|
Definition
| Acidic organelles for degredation and recycling |
|
|
Term
| how do you make the lysosome acidic |
|
Definition
This ATPase is an ATP-dependent H+ pump
The energy of ATP hydrolysis is used to pump H+ into the lysosome |
|
|
Term
| describe Lysosomal enzyme targeting by Mannose-6-P |
|
Definition
1.An enzyme destined for the lysosome is phosphorylated on a mannose sugar in the cis golgi. Where was is made?
2.Mannose-6-P receptors in trans golgi bind this protein and packages it into vesicles
3.Clathrin binds to the outside of these vesicles, targeting them to become lysosomes
4.The lysosomal enzyme is released from the receptor as the lysosome matures
5.Clathrin is released and the receptors are recycled to the golgi
6.Some mannose-6-P receptors that ended up on the plasma membrane are retrieved and recycled. How did they get there? |
|
|
Term
| what are the roles for lysosomes in phagocytosis |
|
Definition
Particles are brought in by endocytosis
The vesicle formed inside the cell is called a phagosome
Lysosomes fuse with phagosomes and transfer their hydrolytic enzymes inside, creating a phagolysosome
The particle gets digested and nutrients pass into the cytoplasm
The leftover, non-digestible material (garbage) is dumped out from residual bodies by exocytosis. This is where some mannose-6-P receptors can make it to the plasma membrane |
|
|
Term
| what are the roles of lysosomes in autophagy |
|
Definition
1. an autphagic vesicle is formed by wrapping ER membranes around a dead mitochondria
2. lysosomes fuse with this to make a autophagolysosome
3. the lysosomes fuse with this to make a autophagolysosome
4. the leftovers remain in the residual body until they can be dumped out of the cell body by exocytosis |
|
|
Term
|
Definition
| a way o get rid of dead organelles such as mitochondria and chloroplasts |
|
|
Term
| how does receptor mediated endocytosis work |
|
Definition
1.Ligands bind to receptors on the outside of the cell. A classic example is LDL (low density lipoproteins) binding to LDL receptors
2.Clathrin binds to the transmembrane receptors and endocytotic vesicles form
3.The clathrin coat is shed, the endosome is acidified, the ligand is dissociated from the receptor and the rest is sorted into different endosomes and other compartments
4.If the ligand is needed by the cell, it is transported to the cytoplasm
5.The receptor is recycled to the plasma membrane
6.If new receptors are needed, they are made in RER and trafficked through the endomembrane system |
|
|
Term
| name 3 events where lysosomal fusion with other membranes occur |
|
Definition
autophagy- mitochondria+ER+lysosome=autophagolysosome
Phagocytosis- phagosome+lysosome=phagolysosome
3.receptor mediated endocytosis-
endocytonic vesiclebecomes and endosome, then lysosome combines to generate a late endosome |
|
|
Term
| name some places where receptors can be found |
|
Definition
1. Plasma membrane
A. Facing outside: LDL receptors
B. Facing inside: t-SNARES
2. Cytoplasm (soluble receptors): importin, SRP
3. Nuclear membrane: Nuclear pore filaments
4. RER
A. Facing cytoplasm: SRP receptor
B. Facing lumen: Cargo receptors
5. Golgi
A. Facing cytoplasm: Transmembrane receptors for COPs
B. Facing lumen: Mannose-6-P receptors
6. Transition vesicles: Transmembrane receptors and v-SNARES |
|
|
Term
| when discussing cellular reproduction what 2 topics are we considering |
|
Definition
| nuclear division(mitosis) and cellular division(cytokinesis) |
|
|
Term
| what was the procedure of the meselson stahl experiments |
|
Definition
1Grow bacteria on “heavy” nitrogen (15N) to metabolically label all DNA
2Then switch to regular “light” nitrogen (14N). All newly replicated DNA will be “light” but the old, parental DNA will be “heavy”
This way you can tell which DNA is new and which is old.
3. Use density gradient centrifugation to separate heavy and light DNA. They actually used cesium density gradients instead of sucrose. |
|
|
Term
| what were the 3 possibilites of the meselson stahl experiments |
|
Definition
1Dispersive: Hybrid in the first generation. Hybrid means ½ light and ½ heavy.
2. Conservative: Always both heavy and light present
3. Semi-conservative: Hybrid in the first generation but both hybrid and light in the second generation |
|
|
Term
| what were the results of the meselson stahl experiment |
|
Definition
1.In the beginning, all of the DNA is heavy (15N)
2.After the first generation, all of the DNA is hybrid because each double stranded piece has one heavy (old, parental) and one new light strand
3.In the second generation, there are hybrid and light bands and there is so little of the original DNA left that it can’t be seen |
|
|
Term
| in what way do bacteria replicate |
|
Definition
|
|
Term
| what are some issues that experimenters must overcome when looking at DNA replication in eukaryotes |
|
Definition
Can’t use gradient density centrifugation to separate chromatids or DNA from eukaryotes so
Use metabolically labeled DNA and look at mitotic chromosomes |
|
|
Term
| what method is used to see DNA replication in eukaryotes |
|
Definition
1.Must use mitotic cells to see compacted chromatids
2.Use BrdU (bromodeoxyuridine) to substitute for thymidine in DNA A:T goes to A:BrdU
3.Thymidine stains dark. BrdU doesn’t.
4.All T is dark, all BrdU is light, hybrid is dark |
|
|
Term
| what are some cell cycle highpoints |
|
Definition
Chromatin is dispersed in interphase for transcription and replication
DNA replication only happens in S phase. Histones and centrioles are replicated in S-phase too in preparation for mitosis
Chromatin condenses into chromatids and forms mitotic chromosomes in mitosis. Since it is condensed, transcription and replication stop. Little or no translation either. |
|
|
Term
| what are some cell cycle exceptions |
|
Definition
No G1 or G2. Most or all of interphase is S-phase. Cells divide a lot but don’t grow much. Much mitotic activity. Examples: Embryonic cells, spermatogonia, etc.
2. Stuck in G1 or Go. No division at all. Terminally differentiated cells such as some neurons, some muscle cells, RBCs, etc.
3. Inducible. Can progress from G1 to S if triggered to do so. For example, lymphocytes can be stimulated to proliferate by exposure to antigens. Liver cells regenerate after injury. Lizard tails can grow back after being cut off. Cancer cells start growing. |
|
|
Term
| what happens to the centrioles during s phase |
|
Definition
they replicate and form the mitotic spindles
the mitotic spindles contains 2 centrosomes,
each centrosome has 2 centrioles |
|
|
Term
| what is happening to the chromatin in mitosis |
|
Definition
| Fibers of DNA and associated protein that constitute chromosomes |
|
|
Term
|
Definition
| Threadlike strands that are composed of the nuclear DNA of eukaryotic cells and are the carriers of genetic information |
|
|
Term
| what do chromatids do during mitosis |
|
Definition
| Paired, rod-shaped members of mitotic chromosomes that together represent the duplicated chromosomes formed during replication in the previous interphase |
|
|
Term
| what are mitotic chromosomes |
|
Definition
| Paired chromosomes compacted into paired chromatids |
|
|
Term
|
Definition
|
|
Term
|
Definition
1. At time 1, the first cells in S-phase pick up radioactivity because they are incorporating 3H thymidine into their DNA as it replicates. It takes them a long time before they are seen in mitosis (all of S and G2).
2. At time 2, cells starting in the middle of S don’t take as long to reached mitosis
3. At time 3, the last cells to leave S phase leave. It doesn’t take them as long to get to mitosis as those at time 2 because they spend less time in S
The time spent between time 1 and time 3 estimates the length of S-phase |
|
|
Term
| Do soluble factors control the cell cycle? |
|
Definition
| Fusion with a cell in S-phase stimulated the G1 cell to go into S-phase. |
|
|
Term
| how would you test for soluble factors within the cell that control the cell cycle |
|
Definition
1.Take out a little of the cytoplasm of an S-phase cell
2.Microinject it into a G1 phase cell. Microinject water into a control G1 phase cell
3.Grow both cells in 3H thymidine, do autoradiography, see if they are radioactive. If the microinjected G1 cell is radioactive, it means it entered S phase |
|
|
Term
| Can G2 cells be stimulated to replicate DNA again? |
|
Definition
| after fusing cells together there was no change seen in the cell |
|
|
Term
| Can G2 cells be affected by M-phase (mitosis) factor? |
|
Definition
: The DNA in the G2 cell started to condense (compact), like they were starting mitosis. Also, G1 can be converted to M and S to M by “M-factor”
Both S-phase and mitosis are controlled by soluble factors
Both S-phase and mitosis are controlled by soluble factors |
|
|
Term
| how do you verify visually if a cell is switching from g1 to a cell in mitosis when fused together |
|
Definition
| G1 chromosomes are compacted due to exposure to the cytoplasm of a mitotic cell |
|
|
Term
| what do we visually see when we Fuse an S-phase cell with a cell in mitosis |
|
Definition
| Since replicating DNA is rather fragile, the M-phase cell factor that tells the DNA to compact causes the S-phase DNA to “pulverize” instead of compacting |
|
|
Term
| what do we visually see when we Fuse a G2 phase cell with a mitotic cell |
|
Definition
| A soluble factor from the mitotic cell causes the G2 chromosomes to condense |
|
|
Term
| What are these soluble factors? |
|
Definition
1.A soluble factor that causes progression from G1 to S
2. Another (different) soluble factor that causes progression from G2 to mitosis |
|
|
Term
|
Definition
Maturation-promoting factor. This stimulates entry into mitosis, as seen by compaction of DNA. MPF is a protein kinase.
Kinases are enzymes that phosphorylate specific proteins |
|
|
Term
|
Definition
| Part of the MPF complex which regulates its activity |
|
|
Term
| how many different kinds of cyclin are there, and what is their relationship to one another |
|
Definition
G1 cyclin stimulates progression from G1 to S-phase
Mitotic cyclin stimulates progression from G2 to mitosis
as g1 increases in concentration to start s phase its concentration goes down, but at g1 also marks the increasing concentration from g2 |
|
|
Term
| will the location of cyclin within the cell affect weather a cell moves to the next phase |
|
Definition
| cyclin b is seen to accumulate in the cytoplasm in the g2 phase, and as mitosis begins the cyclin enters the nucleus |
|
|
Term
| how does cell cycle arrest occur |
|
Definition
1.“Sensors” detect DNA damage or cellular abnormalities
2.The cell cycle is arrested, stalling progression to the next step
3. During this delay, DNA damage is repaired or the cell defect is corrected |
|
|
Term
| what factor stops the cell from continuing |
|
Definition
| CdK inhibitor proteins can act as “molecular brakes” to stop the cell cycle from progressing to the next step |
|
|
Term
| what does the cell look for at the G1 checkpoint |
|
Definition
| the cell checks to make sure the environment is favorable |
|
|
Term
| what does the cell look for at the G2 checkpoint |
|
Definition
| the cells checks to make sure the DNA is replicated and to make sure that all DNA damage is repaired |
|
|
Term
| what does the cell look for at the mitosis checkpoint |
|
Definition
| the cell double checks to make sure that all chromosomes are porperly attached to the mitotic spindle if so the chromosomes get pulled apart |
|
|
Term
| what are the Effects of a mutation in a checkpoint protein |
|
Definition
The brown mouse is a p27 knockout mouse. It has no p27.
Therefore, there is no cell cycle arrest protein to pause progression into S phase.
More S-phase cells, more cell division, more cells, bigger mouse |
|
|
Term
|
Definition
| a CdK inhibitor. It must be removed before the the cell can move into S phase. |
|
|
Term
| what terms are associated with DNA content and ploidy |
|
Definition
Haploid: Single set of genetic information. Single genome
Diploid: Two full sets of genetic information. Two copies of the genome
Polyploid: Many sets of genetic information. Many genomic copies (up to 800 in cotton)
Ploidy (n): Number of sets of genetic information. Number of copies of the genome.
x: Mass of DNA or amount of DNA
c: Number of base pairs (size of DNA)
Human cells are mostly 2n2x2c in G1
x and c number will always be the same |
|
|
Term
| Changes in human DNA content during G1 |
|
Definition
22 autosomes and 1 sex chromosome (XX female or XY male)
That’s 23 kinds of disperse chromatin in G1.
But there are two sets of each because we are diploid (2n) so:
46 pieces of disperse chromatin in G1. They are all linear, double-stranded DNA. |
|
|
Term
| Changes in human DNA content during s phase |
|
Definition
| Each piece doubles so: 92 pieces of disperse chromatin in S-phase. The nucleus is still diploid (2n). Same thing in G2. |
|
|
Term
| Changes in human DNA content during mitosis |
|
Definition
The 92 pieces of disperse G2 chromatin condense in mitosis to form 92 chromatids.
The 92 chromatids are paired to form 46 mitotic chromosomes. Still diploid (2n) |
|
|
Term
| what is going on in a G1 nucleus |
|
Definition
All of the DNA is disperse. Transcription and translation can happen
2n2x2c It is diploid
46 strands of disperse chromatin in G1 |
|
|
Term
| what is going on in the nucleus of an s phase nucleus |
|
Definition
There are 92 pieces of disperse chromatin in S-phase
they are paired to their sister chromatid cohesion holds the pairs together
Still diploid but now
2n4x4c |
|
|
Term
| what is going on in the nucleus of a mitosis nucleus |
|
Definition
Still 92 pieces of double-stranded DNA (chromatin) but now they are compacted as 92 chromatids.
The paired 92 chromatids make 46 mitotic chromosomes
Still 92 pieces of double-stranded DNA (chromatin) but now they are compacted as 92 chromatids.
The paired 92 chromatids make 46 mitotic chromosomes
Paired homologous sister chromatids form 46 mitotic chromosomes |
|
|
Term
| what is going on in the nucleus of a cell during cytokinesis |
|
Definition
Two daughter cells, both diploid (2n2x2c)
Each daughter cell has the same 46 pieces of disperse chromatin in G1 |
|
|
Term
| what is the goal of mitosis |
|
Definition
Make two copies of cells with the same ploidy and DNA content. This is:
Equational Division (no change in n) |
|
|
Term
|
Definition
helps to keep the two pieces of chromatin together after S-phase, through G2 and into the beginning of prophase
Phosphorylation of cohesin in early prophase causes a loss of cohesin between homologous chromatids except near the centromere
its like the clip in you hair |
|
|
Term
|
Definition
| helps to compact and supercoil DNA in prophase |
|
|
Term
| What phases of the cell cycle would have the most condensin associated with chromatin? |
|
Definition
| Prophase, prometaphase, metaphase, anaphase |
|
|
Term
| Which phases of the cell cycle would have the most cohesin associations with chromatin? |
|
Definition
|
|
Term
| what provides a scaffold to hold the DNA in the mitotic chromosomes |
|
Definition
| condensin cohesin and other proteins helps to hold the DNA in the mitotic chromosomes |
|
|
Term
| how do mitotic spindles form |
|
Definition
1. Pericentriolar material surrounding centrioles serves as the nucleation site (MTOC) for cytoplasmic microtubules
2. The initial spindle pole forms outside of the nucleus
3. Breakdown of the nuclear envelope, ER and golgi |
|
|
Term
| How can you tell you’re in prophase? |
|
Definition
1.Mitotic chromosomes are seen but they aren’t clustered near the middle
2.MTs from the mitotic spindle (aster) have not made contact with any chromosomes |
|
|
Term
| In which phase of the cell cycle would you see centrioles inside the nucleus? |
|
Definition
|
|
Term
| what happens in prometaphase |
|
Definition
1. A protein complex on the centromere is called the kinetochore.
2. The plus ends of chromosomal MTs start to “capture” mitotic chromosomes at their kinetochores
3. Mitotic chromosomes begin to move (oscillate) and end up near the spindle equator at the end of prometaphase
4. Sister chromatids end up in amphitelic orientation. Each faces opposite poles. |
|
|
Term
|
Definition
| a protein complex that is attached to the centromere |
|
|
Term
| Is the kinetochore always at the center of human mitotic chromosomes? |
|
Definition
|
|
Term
|
Definition
| Eminate from centrosome into cytoplasm to anchor and position the aster (mitotic spindle) |
|
|
Term
|
Definition
| connect from pericentriolar material of centrosome to kinetochores |
|
|
Term
|
Definition
| Extend from centrosome to equator but interact with other polar MTs instead of chromosomes |
|
|
Term
| what are Three main forces for movements in prometaphase |
|
Definition
1. Dynein and kinesin-like motors on the kinetochore corona fibers to grab the MT and position it
2. Polymerization and depolymerization of tubulin to lengthen and shorten MTs
3.“Cargo and rail” action of motor proteins on MTs to position chromosomes and poles |
|
|
Term
| Can there be any movements of mitotic chromosomes in prometaphase if there was no ATP? |
|
Definition
Polymerization and depolymerization of tublin, no energy required,
Cargo and rail action of motor proteins on microtubule to position chromosomes
Therefore no atp movement in prometaphase is possible |
|
|
Term
| What if there was no GTP? |
|
Definition
| gtp is required for movements in prometaphase |
|
|
Term
| what does the relationship between kinetochore and coronal fibers and its benefit to move chromosomes |
|
Definition
| It helps to move and position the mitotic chromosomes |
|
|
Term
| Can chromosomal MTs shorten at both the plus and minus ends? |
|
Definition
| The coronal fibers attach to the dam ring, sits around the microtubule so that the chromosome is pulled as the microtubule is depolemerized, then the use of depolemerase breaks down the plus end near the dam ring. Depolymerization also occurs at the spindle poles due to depolymerase |
|
|
Term
| what is the role of motor proteins in mitosis |
|
Definition
| position the mitotic chromosomes and the poles |
|
|
Term
| name 3 ways to properly position the dna of a cell |
|
Definition
1.Polar spindle fiber MT sliding by kinesin causes the poles to move apart
2.Dynein-based movement moves mitotic chromosomes toward the minus ends of chromosomal spindle fibers
3.Kinesin-based movement moves mitotic chromosomes toward the plus ends of chromosomal spindle fibers |
|
|
Term
| what occurs during metaphase |
|
Definition
Mitotic chromosomes align in amphitelic orientation at the metaphase plate.
Amphitelic means that each one of the two sister chromatids face opposite poles
This is in the middle (equator) of the mitotic spindle.
Colchicine and colcemid (inhibitors of MT polymerization) produces metaphase chromosomes because it stops them from being pulled apart in anaphase |
|
|
Term
| How can you tell you’re in metaphase? |
|
Definition
| chromosomes are alligened along metaphase plate, attached by chromosomal microtubules to both plates |
|
|
Term
| are microtubules dynamic during mitosis |
|
Definition
| The rate of tubulin addition is similar to the rate of loss so the MTs “treadmill” in metaphase |
|
|
Term
| How do you know you’re in anaphase? |
|
Definition
| Sister chromatids have come apart but they aren’t very close to the poles yet |
|
|
Term
| what does the spindle checkpoint do |
|
Definition
assures that all mitotic chromosomes reach the spindle equator before anaphase begins
if this check point fails may cause genetic instability |
|
|
Term
| what is happening in anaphase a |
|
Definition
| the loss of chromosomal microtubules inorder to move the chromatids, no atp required |
|
|
Term
| what is happening in anaphase b |
|
Definition
| polar microtubules are beign added and kinesin is moving these polar microtubules inorder to push the poles apart |
|
|
Term
|
Definition
They both act by turning off existing signals
They are both multisubunit enzyme complexes.
They cause ubiquitination of many substrates.
A substrate is what an enzyme acts upon.
Ubiquitination attaches ubiquitin to a substrate.
SCF and APC ubiquitinate different substrates.
Ubiquitination labels substrates for destruction.
A substrate with ubiquitin on it is targeted for degredation.
SCF and APC don’t destroy proteins themselves, they target the proteins for destruction by other processes |
|
|
Term
|
Definition
| (S-phase control factor) helps start S-phase but goes away in anaphase |
|
|
Term
|
Definition
| Anaphase promoting factor) has two types, one peaks during anaphase and the other starts at anaphase and ends at S-phase |
|
|
Term
|
Definition
1.It targets the destruction of some proteins that hold chromatids together (securin), allowing progression from metaphase to anaphase
2.Since mitotic cyclins keep cells in mitosis, destroying them enables progression into G1 |
|
|
Term
| whats the point of all these regulation proteins |
|
Definition
| The cell cycle can be regulated not only by the appearance of controlling factors, but also by their regulated disappearance |
|
|
Term
| Two ways to decrease protein amounts |
|
Definition
decrease synthesis or increase degradation
SCF and APC can specifically target proteins for degradation by ubiquitination |
|
|
Term
| what are some ways to regulate proteins involved in the cell cycle |
|
Definition
1.Change their amounts
A. Change rate of transcription or translation
B. Change rate of degredation
2. Change their locations
A. Move them, target them, anchor them
3. Change their activites
A. Covalent modifications (like phosphorylation) |
|
|
Term
| How do you know you’re in telophase? |
|
Definition
| Chromatin becomes disperse and clustered near the poles. No mitotic chromosomes seen |
|
|
Term
| what happens in cytokinesis |
|
Definition
1.Contractile ring forms to pinch off cell at the center. This is microfilaments and myosin II
2.Two daughter cells produced, each in G1
3.Each cell has 46 strands of disperse chromatin.
4.Each is 2n2x2c. They are diploid |
|
|
Term
| what is the goal of meiosis |
|
Definition
reduction devision
2n4x4c--1n2x2c---1n1x1c |
|
|
Term
| what is the goal of sexual reproduction |
|
Definition
| return to the diploid state |
|
|
Term
|
Definition
| is nuclear division (equational division). There is an S-phase in between the next mitosis |
|
|
Term
|
Definition
is 2 nuclear divisions with no S-phase in between (reduction division)
Signals received in pre-meiotic cells trigger them (in G1) to start pre-meiotic S-phase. In other words, the decision about whether to go into mitosis or meiosis is made in G1.
Pre-meiotic G2 cells have 2n4x4c but pre-meiotic G2 cells are a little different than pre-mitotic G2 cells |
|
|
Term
| what is primary meiocvtes |
|
Definition
are cells that have just come out of pre-meiotic G2 and have entered prophase I of meiosis
Meiotic prophase nuclei differ from mitotic prophase nuclei due to formation of synaptonemal complexes and bivalents (tetrads) in meiotic prophase I |
|
|
Term
| what is a mitotic chromosome |
|
Definition
it is paired sister chromatids
both chromatids are generally identicla
same thing in meiosis but it will be known also as meitotic chromosomes |
|
|
Term
| what are bivalent(tetrad) in meiosis |
|
Definition
homologous chromosomes(homologous meitotic chromosomes)
paired meitotic chromosomes
both meiotic chromosomes carry similar information but they are not genetically identical |
|
|
Term
| Bivalents (tetrads) in meiosis |
|
Definition
It is bivalent because it is two meiotic chromosomes
It is a tetrad because it has four chromatids
It is syntelic because both sister chromatids face the same pole |
|
|
Term
| what happens in Leptotene (first part of meiotic prophase I) |
|
Definition
Compacted meiotic chromosomes become visible
Each is a pair of identical chromatids (from S phase duplication)
There are 46 compacted meiotic chromosomes |
|
|
Term
| How can you tell that this is meiotic prophase I and not meiotic prophase II? |
|
Definition
twice as much dna in prophase 1, 1/2 as much in prophase 2
no bivalents in leptotene |
|
|
Term
| what is the goal of meiosis |
|
Definition
|
|
Term
| what happens in zygotene of meiotic prophase 1 |
|
Definition
A process called synapsis starts to pair homologous chromosomes
Homologous chromosomes are held together by synaptonemal complexes
Paired homologous chromosomes are called bivalents or tetrads |
|
|
Term
| what is the role of synaptonemal complexes in prophase 1 of meiosis 1 |
|
Definition
| Homologous chromosomes are held together by synaptonemal complexes |
|
|
Term
| what happens in Pachytene of meiotic prophase I |
|
Definition
Synapsis ends, synaptonemal complexes are fully formed
Some genetic recombination is starting to be seen |
|
|
Term
| what happens in diplotene |
|
Definition
Synaptonemal complexes break down
Homologous chromosomes held together by chiasmata (plural of chiasma)
A chiasma is a crossover point between non-sister chromatids. It is a covalent attachment. |
|
|
Term
|
Definition
covalent linkages between two non-sister chromatids. This helps to keep bivalents together after cohesion linkages are broken
Chiasmata are also sites of genetic recombination by crossovers |
|
|
Term
| what happens in Diakinesis of meiotic prophase I |
|
Definition
Meiotic spindle forms. This is similar to the mitotic spindle
Some further compaction of the chromosomes can occur
Chiasmata continue to hold homologous chromosomes together, even into metaphase
The nuclear envelope begins to break down and spindle MTs begin to contact the chromosomes |
|
|
Term
| How can you tell this is prophase I of Meiosis I and not prophase II of meiosis II? |
|
Definition
| bivalents are seen after leptotene |
|
|
Term
| how does recombination occur |
|
Definition
| Crossing-over and recombination occurs between non-sister chromatids in pachytene |
|
|
Term
| Are synaptonemal complexes seen throughout prophase I of Meiosis I? |
|
Definition
| No. Only in zygotene and pachytene |
|
|
Term
| what are some differences in the alignment of the dna in mitosis and meiosis |
|
Definition
In mitosis, copies of each chromatid align at the metaphase plate
In meiosis, copies of each meiotic chromosome align at the metaphase plate |
|
|
Term
| when you pull apart cells in mitosis in anaphase what is the result |
|
Definition
Paired sister chromatids
Both chromatids are genetically identical
Same thing in meiosis but we’ll call it a meiotic chromosome for clarity |
|
|
Term
| when you pull apart cells in meiosis(bivalent(tetrad) in anaphase what is the result |
|
Definition
Homologous Chromosomes (homologous meiotic chromosomes)
Paired meiotic chromosomes
Both meiotic chromosomes carry similar information but they are not genetically identical |
|
|
Term
| give your best description of the dna of cells in meiosis |
|
Definition
It is bivalent because it is two meiotic chromosomes
It is a tetrad because it has four chromatids
It is syntelic because both sister chromatids face the same pole |
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Term
| what is the goal of meiosis |
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Definition
haploidization
by use of meiosis 1 and 2 |
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Term
| review concept, can you list the changes in n,x,c of the dna as you change form in meiosis |
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Definition
First meiotic division (Meiosis I):
Homologous chromosomes pair as bivalents or tetrads (2n4x4c)
Intact meiotic chromosomes (as paired chromatids) separate
No S-phase in between
Second meiotic division (Meiosis II):
Homologous chromatids separate
Each nucleus gets one set of chromatids
Four haploid gametes, all 1n1x1c |
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Term
| How could you tell that this isnt prophase of mitosis |
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Definition
| - if you can see paired miotic chromosomes in prophase you are in meiosis |
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Term
| what is going on in the leptotene phase (first part of meiotic prophase I) |
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Definition
Compacted meiotic chromosomes become visible
Each is a pair of identical chromatids (from S phase duplication)
There are 46 compacted meiotic chromosomes |
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Term
| How can you tell that this is meiotic prophase I and not meiotic prophase II? |
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Definition
| twice as much dna in prophase 1, 1/2 as much in prophase 2 |
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Term
| what are 2 source of genetic variability in normal meiosis |
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Definition
1. crossing over and recombination
2. independent assortment |
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Term
| what is crossing over and recombination |
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Definition
This happens in pacytene of prophase I
It changes DNA sequences of chromatids |
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Term
| what happens in independent assortment |
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Definition
| mix and match the dna as they separate from the maternal paternal cells, no crossing over , happens in pacytene of prophase 1 |
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Term
| what is aneuploidy and how does it occur |
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Definition
Abnormal number of chromosomes
this is not supposed to happen
Aneuploidy can result from either primary or secondary nondisjunction |
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Term
| give some examples of aneuploidy |
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Definition
All of these are caused by nondisjunctions during meiosis
Autosomal polyploidy. This is usually fatal except in the case of trisomy 21 (three chromosome #21)
2. Autosomal monosomy. Only one of the autosomes instead of two. This is usually fatal
Sex chromosome polyploidy.
XXY is male with Kleinfelter’s syndrome
XYY is male and was previously thought to have criminal tendencies because of being “too male”
4. Sex chromosome monosomy.
XO is female with Turner syndrome |
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Term
| compare and contrast mitosis and meiosis in both their goals and methods of achieving their goals |
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Definition
Mitosis produces daughter cells with the same genotype as the mother cell
No genetic segregation or independent assortment in mitosis
Meiosis produces cells with different mixtures of maternal and paternal genes because of:
Independent assortment
Genetic recombination
Independent assortment and recombination happen in meiosis, not mitosis
Goal of Mitosis:
Faithful division of DNA so the daughter cells are genetically identical to the mother cell. Keep it real, keep it diploid.
Goal of Meiosis:
Mix it up. Produce haploid gametes with different genetic contributions from maternal and paternal sources for further genetic mixing by sexual reproduction. |
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Term
| describe the pathway to make a sperm cell |
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Definition
1.start with a primary spermatocytes (2n4x4c)
2.use meiosis1
3. now you have a Secondary spermatocyte (1n2x2c)
4. use meiosis 2
5. you should now have Spermatids (1n1x1c)
6. differentiation is used
7.- sperm cells(1n1x1c) are produced |
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Term
| describe the pathway to get to the egg cell |
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Definition
1. diferentiation occurs
2. primary oocyte is formed(2n4x4c)
3. meiosis 1
4. secondary oocyte (1n2x2c) is formed
5. use meiosis 2
6. you now have a polar body and egg cells each at (1n1x1c) |
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Term
| what is special about fungi |
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Definition
In fungi, the adults are haploid
Meiosis occurs right after fertilization |
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Term
| describe Plants, Sporic or intermediate |
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Definition
| In plants, the gametophytes can generate gametes by mitosis instead of using them for fertilization |
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Term
Do all DNA mutations cause protein changes?
What could a change from Q to K do? |
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Definition
a single change may or may not be harmfull due to the silent mutation of the third base pair, and the ability to code for one protein for many base pair combinations
how ever if there is a change in the protein depending on the position and charge of that protein the protein could become mishapen. this can be good or bad depending on how the body copes with these changes |
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Term
| where do somatic cells come from |
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Definition
| Somatic cells come from one parental cell type. Germ-line cells come from the fusion of gametes |
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Term
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Definition
Spontaneous change in DNA sequence leading to a change in amino acid sequence of this gene product
Only mutations in germ-line cells are passed on to the progeny |
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Term
What’s the point of point mutations?
Are all mutations bad? |
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Definition
| Point mutations can be either bad, good or do nothing |
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Term
| can you produce an example of a mutation process |
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Definition
1.Since the mutant can’t make histidine, it can only grow if histidine is added, This is a His- mutant.
2.The rate of spontaneous mutations is about 1 in 109 nucleotides copied
3.If you screen enough of these bacteria, eventually you can get a revertant that restores normal function |
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Term
| DNA damage and replication mistakes happen. What to do about it? |
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Definition
1. Proofreading by DNA polymerase I
2. Nucleotide excision repair
3. Base excision repair
4. Double-strand break repair |
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Term
| What happens if you can’t repair the mistake? |
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Definition
Either cell death, suicide (apoptosis) or the DNA mutations can be passed on during replication.
A. Germ cell: Genetically inherited mutation (not always bad)
B. Somatic cell: Cancer |
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Term
| how do you Edit and correct dna damage using DNA polymerase I |
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Definition
DNA polymerase I replicates eukaryotic DNA
This enzyme has a proofreading capability, where mismatched bases are excised and corrected
However, some mistakes can get through
The error rate during DNA replication is the spontaneous mutation rate |
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Term
| how do you repair A pyrimidine dimer that has formed within a DNA duplex following UV irradiation |
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Definition
Nucleotide excision repair (NER) removes bulky lesions, such as thymine dimers and chemically altered nucleotides.
1. DNA damage is recognized by a protein complex
2. The helicase activity unwinds the DNA
3. It cuts it
4. It removes the damaged sequence
5. The gap is filled by a DNA polymerase
6. The DNA is rejoined by a ligase |
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Term
| how does base excision repair work |
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Definition
DNA glycosylase recognizes the alteration and cleaves the base from the sugar.
An endonuclease cuts the DNA open
A polymerase fills the gap by inserting a nucleotide complementary to the undamaged strand.
The strand is sealed by DNA ligase.
At least 4 enzymes are necessary for this. That’s 4 chances at problems due to inability to fix DNA problems |
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Term
| Repairing DSBs by nonhomologous end joining (NHEJ) |
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Definition
Ionizing radiation (X-rays, gamma rays) along with some chemicals cause double-strand breaks (DSBs).
DSBs can be repaired by a pathway in mammalian cells in which proteins bind to the broken ends and catalyze reaction to rejoin the broken ends.
Cells that lack one of the Double-strand breakage repair proteins required for NHEJ are very sensitive to ionizing radiation.
Defects in this repair pathway have been linked to increased cancer susceptibility. |
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Term
Why have apoptosis?
How prevalent is it? |
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Definition
Cell necrosis is ugly and messy. It generates all sorts of garbage Apoptosis is a neat and orderly way to kill cells
alot of cells die each day in our bodies due to apoptosis |
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Term
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Definition
An example of the use of mutations in experiments to identify key enzymes in a biochemical pathway
Beadle-Tatum experiments with Neurospora (bread mold)
essentially use spores of bread mold and irradiate with x rays or uv light and grow the spores on a variety of supplemented medium to figure out what is important on a specific metabolic or chemical pathway |
|
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Term
| name 2 other kinds of genetic mutations |
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Definition
Change in DNA sequence in another region that regulates the level of expression of this gene
Change in the number of copies of a gene, possibly producing more of the gene product or a template for further mutations and a new gene |
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Term
| what happens when misalignment occurs during genetic recombination |
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Definition
Unequal crossing-over can produce mutated chromosomes in prophase I
Some gametes could get an abnormally long or short chromosome |
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Term
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Definition
Exons are the coding regions, introns are the sequences in between
exons can be swapped from another gene |
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Term
| what happens during horizontal gene transfer |
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Definition
DNA from one organism can be transferred to another and become part of the genome
this is what we saw in the griffith experiment, the dna of the killers mixed with the non killers resulting in the uptake of the killer genes giving the non killers the ability to kill
another example would be HIV, it changes because they use horizontal gene transfer to pass on resistance |
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Term
describe horizontal gene trasfer by the retrovirus
Will this genetic defect be passed on to the progeny if the viral DNA is dormant? |
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Definition
1. The HIV virus binds to an HIV-sensitive cell
2. HIV RNA is reverse-transcribed into DNA
3. The HIV DNA is integrated into the genome
4. It can either stay dormant or be expressed
5. When it is expressed, it makes more viruses, kills the cell and releases
many more viruses
yes |
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Term
| Can HIV infect germ-line cells? |
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Definition
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Term
| describe Apoptosis and removal of the dead cell by a macrophage |
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Definition
Apoptosis generates caspases which are specific proteases.
Examples of the target proteins for these caspases are protein kinases, nuclear lamins, cytoskeletal proteins and DNase
Caspases can be activated to cause apoptosis by either an extrinsic pathway (stimulated by receptors) or an intrinsic pathway |
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Term
| where do we see programed death |
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Definition
during development apopotosis is used to clear up webbing between fingers
in neurons, some neurons are meant to die if it is found that the connection they make is not essential. the target cell releases a survival factor that prevents the neuron from dieing resulting in neurons that fire together wire together. wireing here means the neurons stays alive becaause it is beign used and absorbing the survival factors that the target cell is producing |
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Term
| list some of the effects of DNA damage |
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Definition
1. DNA gets damaged by radiation, mutagens, etc.
2. BRCA enzymes help repair the damage.
If they are mutated or missing, damage persists
3. A checkpoint should catch this damage and activate p53
4. p53 is a transcription factor that triggers either:
p21 expression and cell cycle arrest or
apoptosis |
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Term
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Definition
(a) Cell division does not normally require p53
(b) If DNA is damaged (like by a mutagen), p53 levels rise
p53 acts to either arrest the cell in G1 or go into apoptosis
(c) If no p53 and no cell arrest, the cells proceed to either a tumor or death |
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Term
| what is another way to cause apopotosis |
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Definition
| cell damage can activate bax, bax cause cytochrom c to be released from mitochondria, executioner caspases get activated and apopotosis occurs |
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Term
| is there a way to stop apopotosis |
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Definition
a survival factor binds to membrane receptor of the plasma membrane
bc12 gene transcription is activated, and bc 12 protein block apoptosis
but if the gene is mutated it may not have the ability to block apoptosis |
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Term
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Definition
Cancer is usually due to somatic genetic mutations that are not heritable.
(You may inherit a genetic predisposition for it though.) |
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Term
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Definition
| They ignore inhibitory signals (like checkpoints). For example about 50% of human cancers have altered p53 |
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Term
| what are tumor suppressor genes |
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Definition
| They don’t need stimulatory signals for cell division |
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Term
| Is p53 just made and degraded constantly if no DNA damage? |
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Definition
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Term
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Definition
once it seses there is dna damage, p53 gets activated causing it to bind with dna to transcribe gene 21
gene21 makes p21 a cdk inhibitor which causes cell cycle arrest by inactivating the soluble factor that sends the cell into the next phase |
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Term
| what are some ways to trigger cancer |
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Definition
1. Mutate BRCA enzymes. DNA damage not repaired properly
2. Mutate p53. Less expression of p21 and loss of checkpoint control
3. Mutation in p21. Inability to respond to p53 and loss of checkpoint control
4. Increased MDM2 causing ubiquitination of p53, loss of p53, loss of checkpoint control
BRCA, p53 and p21 are tumor suppressor genes
MDM2 can accelerate cell division |
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Term
| what is One way for a mitogen to trigger cancer |
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Definition
G1-Cdk and G1/S-Cdk are kinases that trigger progression into S-phase
Activation of these kinases causes phosphorylation of a protein that keeps a transcription regulator inactivated
Genes get transcribed that produce proteins to stimulate cell division |
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Term
| why is cancer hard to cure |
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Definition
| some times many mutations are required to cause a cell to go cancerous and there are many ways to make the cell cancerous leading to a variety of causes and symptoms making it difficult to cure |
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Term
what are telomeres
and what are the roles of telomeres |
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Definition
bits of dan that is tacked on to the ends of dna
When the telomeres are gone, there are problems with DNA replication and
shortening of DNA strands. Cells deal with this by:
Ceasing to divide (replicative senescence)
Checkpoint arrest and DNA repair
Expressing telomerase to extend telomere length
Apoptosis, cancer or cell death
telomerase can create more telomers
elongation of telomers can be an indication of cancer |
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Term
| compare mutagens and mitogens |
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Definition
mitogens trigger mitosis and cell division
mutagens change DNA producing mutations |
|
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Term
| what are possible signals for differentiation |
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Definition
| genetic factor or epigenetic factors |
|
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Term
| what is pluripotant stem cell |
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Definition
| A pluripotent stem cell can give rise to any kind of cell that can be made from that organism’s genomic DNA |
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