Test2day2 Flashcards

1
Q

What separates in anaphase of mitosis?
What separates in anaphase of meiosis one?
What separates in anaphase of meiosis two?

A

sister chromatids
homologous chromosomes
sister chromatids

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2
Q

The place where maternal and paternal chromosomes have exchanged DNA is called a ___

A

Chiasma

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3
Q

N+1 N+1 N-1 N-1 occurs from nondisjunction at what stage?

N+1 N-1 N N occurs from nondisjunction at what stage?

A

Metaphase in meiosis 1

Metaphase in meiosis 2

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4
Q

The insulin like growth factor is only expressed from the gene inherited from the father. What type of imprinting is this?

A

Maternal because the mom’s gene is silenced

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5
Q

What is uniparental disomy?
Heterodisomy occurs how?
Isodisomy occurs how?

A

When someone receives two copies of a chromosome from one parent, and none from the other.
Nondisjunction at meiosis 1 (Pair of non-identical chromosomes is inherited from one parent)
Nondisjunction at meiosis 2 (Single chromosome from one parent is inherited)

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6
Q

Which chromosome does Prader Willi syndrome have an effect from? Also, explain why this disease occurs and how it relates to genomic imprinting

A

15
The maternal copy of this gene is imprinted (so mother’s genes are silenced). The disease occurs when the fathers genes, that are suppose to be the only ones expressed, are either deleted or also silenced. Then, there is no expression at all of these genes on chromosome 15. Isodisomy is one way this can occur (If the genes inherited are only the mothers, but since it’s silenced, no gene expression at all).

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7
Q

___ is the idea that females have x-inactivation of one of their x-chromosomes so that they don’t have twice as many x gene products as males

A

Lyonization

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8
Q

Name the phases of interphase and what they do

A

G1 - RNA and protein synthesis needed for DNA replication
S phase - DNA is replicated (synthesized)
G2 - DNA stability is checked and cell prepares to divide

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9
Q

When a cell passes the ___ it becomes growth factor independent. Also, where is this located?

A

Restriction point, G1 phase

(If not enough growth factors present, the cell does not pass through the restriction point. Once it does however, it is no longer dependent on growth factors)

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10
Q

Name the checkpoints

1) Makes sure the chromosomes were duplicated correctly before committing to mitosis.
2) Ensures chromosomes are attached to the mitotic spindle
3) Corrects any DNA damage (such as that from chemical modifications like methylation) before continuing

A

1) G2 checkpoint
2) M checkpoint
3) G1 checkpoint

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11
Q

Initiation of S phase protein synthesis requires the transcription factor ___

A

E2F

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12
Q

Take the question step by step.

In order to get past the G1 checkpoint, Myc must activate cyclin __ and CDK __ or __.The enzyme responsible for the complete activation of the cyclin-CDK complex is ____; now, this active complex must phosphorylate __, inactivating it and releasing the transcription factor ___, which then goes on to activate cyclin __ and CDK __ which allows the transition from G1 to S to be accomplished. Cyclin __ and CDK __ is responsible for the continuation of the S phase and both of these 2 Cyclin-CDK complexes that were activated by E2F keep the RB phosphorylated so it cant become active again. In order to activate mitosis, cyclin __ or ___ and CDK ___ is active

A

d, 4 or 6, CAK (CDK-activating kinase), Rb (retinoblastoma protein), E2F, E, 2, A, 2, A, B, 1

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13
Q

Normally, cyclin-CDK is activated by phosphorylation from CAK, however, if the complex is phosphorylated again at the roof site of CDK, it is deactivated. What is this enzyme called that phosphorylates it for a second time? The cyclin-CDK complex can have its second phosphate group removed to reactive it (now it’ll only have one phosphate group aka the active one). What enzyme can remove the second added phosphate?

A

Wee1 Kinase

Cdc25 phosphotase

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14
Q

What is the role of p27?

A

It binds to the cyclin-CDK complex to inhibit its kinase activity (belongs to a group of CDK inhibitors called CKIs)

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15
Q

Proteolysis (protein degradation) can be a way of degrading cyclin proteins. The progression of metaphase to anaphase is triggered by protein destruction due to the ___ complex

A

APC/C (Anaphase promoting complex or cyclosome)

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16
Q

What does the activation of P53 do?

A

P53 activates CKI,s (like P27, P21 etc.) which bind to cyclin-CDK complexes to stop the cell cycle at G1 so it can enter G0 and be repaired. (In short, DNA damage leads to p53-mediated cell cycle arrest at the G1 checkpoint)

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17
Q

Which apoptosis pathway is mitochondrial dependent?

A

Intrinsic pathway

18
Q

The trimeric association of the FAS receptor causes activation of ___.

A

caspases

19
Q

__ is released from the mitochondria when apoptosis must occur. This binds to APAF-1, which forms a ___, and this goes on to activate which caspase which goes on to further activate caspase __

A

Cytochrome C, Apoptosome, 9, 3

20
Q

Which two proteins activate apoptosis in the intrinsic pathway?
Which one deactivates it?

A

Bax and Bak

BCL

21
Q

c-SRC is an example of a ___, and if it’s converted to v-SRC, it is now considered a ___

A

Proto-oncogene, oncogene

22
Q

__ is the name for sperm binding receptors for the cortical reaction to occur. Also, if there is a mutation in __ the sperm can not fuse to the egg and undergo the acrosomal process

A

ZP3, Izumo

23
Q

When a single fertilized egg splits, it is called __.

When two separate eggs are fertilized it is called ___

A
Monozygotic twins (identical)
Dizygotic twins (fraternal)
24
Q

The presence of two or more populations of cells with different genotypes in one individual who has developed from a single fertilized egg is called ___.
Two or more genotypes arise from the fusion of more than one fertilized zygote in the early stages of embryonic development is called ___

A

Mosaicism

Chimera

25
Q

Zygote -> 2,4, then 8 cell stage (what is this stage called)? -> Morula -> blasatocyst with an inner cell mass called ___ and an outer cell mass called ___

A

cleavage, embryoblast, trophoblast

26
Q

Embryonic stem cells are derived from what ?

Also, what kind of potency do they have?

A

Inner cell mass aka embryoblast
They are considered pluripotent because they can only give rise to cell types that make up the body. Embryonic cells at the 2,4, or 8 cell stage (right after the zygote is formed) are totipotent because they can give rise to body cells, and extraembryonic or placental cells.

27
Q

What two layers to do trophoblasts and embryoblast differentiate into?

A
Trophoblast = Synctiotrophoblast and cytotrophoblast
Embryoblast = Epiblast and hypoblast
28
Q

What hormone is secreted to maintain the embryo and make sure endometrial lining is not lost? What layer secretes it?

A

hCG, syncytiotrophoblast

29
Q

When implantation occurs somewhere else, what is it called?

A

Ectopic

30
Q

When in development does this occur?

1) Not susceptible to tetratogens (Anything that can cause a congenital birth defect)?
2) CNS
3) Heart
4) Upper limbs
5) Lower limbs
6) Eyes
7) Ear
8) Palate
9) Teeth

A

1) First two weeks since it’s not attached to the placenta
2) 3-16
3) 3-6
4) 4-6
5) 4-6
6) 4-8
7) 4-9
8) 7-8
9) 7-8

31
Q

What is the source of all three germ layers?

A

Epiblast

32
Q

What is the first future axis of the embryo? Also, what growth factor initiates and maintains this formation?
What eventually takes over as the second axis of the embryo?

A

The primitive streak, Nodal, notochord (forms in the mesoderm layer)

33
Q

Which arm is above the centromere and which is below on a chromosome?

A

P arm above, Q arm below

34
Q

Name the type of cell signaling

1) Used for long distance signaling
2) Acts locally
3) Secreting cells themselves express cell surface receptors
4) Ligand stays attached to signaling cell and binds to a receptor on an adjacent target cell

A

1) Endocrine
2) Paracrine signaling
3) Autocrine signaling (like in growth factors)
4) Direct signaling (FAS death receptor)

35
Q

GEFs ___ g proteins, where as GAPs ___ g proteins

A

Activate (Exchange GTP for GDP), deactivate (Make g protein lose GTP)

36
Q

Name the steps in GPCRs for GsAlpha and GqAlpha

A

Ligand binds -> Receptor binds G-protein -> Receptor acts as a GEF and causes GTP to bind to G-protein as GDP is lost -> Alpha subunit of G protein is active -> Adenylyl cyclase active -> catalyzation of cAMP -> cAMP activates PKA -> PKA can phosphorylate target proteins to alter their activity

Ligand binds -> Receptor binds G-protein -> Receptor acts as a GEF and causes GTP to bind to G-protein as GDP is lost -> Alpha subunit of G protein is active -> Phospholipase C (PLC) active -> PIP2 cleaved -> IP3 and DAG produced -> IP3 causes Ca2+ release from ER -> Ca2+ causes Protein kinase C (PKC) to translocate to the plasma membrane and is activated by DAG -> Phosphorylation of target proteins to alter the activity

37
Q

What cause the cholera epidemic?

A

G alpha is not able to hydrolyze GTP -> GDP, so it can’t turn off. Therefore, cAMP continues to be made -> PKA continues to be made -> PKA phosphorylates the CFTR Chloride channel -> Since cl- continues to be pushed out, water follows it and it makes you loose all your water

38
Q

Potentiate means what ?

Attenuate means what?

A

Turn up

Turn down

39
Q

What removes cAMP and cGMP?

A

Phosphodiesterases (PDE) so if one is broken, then the amount of cAMP or cGMP will not be lowered

40
Q

Desensitization can occur when G protein receptor kinases (GRKs) phosphorylate the GPCR. When phosphorylated, __ binds to to GPCR so that it can not bind a g-protein and convert GDP -> GTP.

A

arrestin

41
Q

Name the steps in RTKs

A

Ligand binds (growth factor) -> Causes dimerization of receptor to phosphorylate itself on the tyrosine residues -> SH2 domains bind to phosphotyrosines (GRB2 is the protein in mammals) -> GRB2 has SH3 domains on the other side of it, which binds to SOS (a GEF) -> SOS binds to RAS and acts as a GEF to cause GDP displaced and GTP binding -> RAS binds to RAF -> MAP kinase pathway activated (RAF -> MEK -> ERK ) -> Phosphorylation of protein targets leads to alterations in gene transcription and protein activity

42
Q

Explain mechanism for RAS dependent and independent signaling for insulin

A

RAS dependent: Insulin binds to RTK -> Dimerization and autphosphorylation -> Insulin receptor substarte 1 (IRS-1) binds to phosphotyrosines -> GRB 2 binds to IRS-1 -> RAS activated -> alterations in gene transcription

RAS independent: Insulin binds to RTK -> Dimerization and autphosphorylation -> Insulin receptor substarte 1 (IRS-1) binds to phosphotyrosines -> PI3K binds to IRS-1 -> PKB activated -> alterations in protein and enzyme activity