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Biol 202 > Lecture 27 > Flashcards

Lecture 27 Flashcards

1
Q

What is dosage compensation and what is the type of inheritance?

A

It is when in a female in each cell an X chromosome is inactivated= epigenetic inheritance
the fur of calico cats is due to this phenomenon

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2
Q

What are different mechanisms for the X inactivation

A
  • either like the X chromosome in the male is over expressed due to a lot more histone acetylation
  • either in the X chromosomes of the female you have more histone methylation and acetylation and in the males you have a lot more acetylation
  • one X chromosome is silenced in the female and the male has more acetylation
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3
Q

What are the consequences of histone acetylation and what catalizes it?

A
  • Histone tail acetylation on lysines neutralizes positive charge, loosens interaction with DNA (negative charge) = chromatin relaxation= increased accessibility and transcription
  • created binding sites for histone code readers that help promote activation
  • HAT which is a transcriptional co-activator
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4
Q

Histoner acetylation is removed by what?

A

histone deacetylase that are transcriptional co-repressors

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5
Q

histone tails can be methylated by what?

A

histone methyltransferase (HMTase) enzymes ex: H3K9Me

  • does not change the charge of the histone
  • histone methylation marks aka H3K9Me are associated with gene silencing and acts as a signal to recruit specific readers
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6
Q

What is the role of H3K9Me?

A
  • Promotes heterochromatin formation and tends to spread on chromatin
  • HP-1 binds methylated histones due to H3K9Me
  • HP-1 promotes heterochromatin formation and recruits more HMTases…..
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7
Q

How is the spread of heterochromatin stopped?

A

-heterochromatin spreading is conteracted by HATs bound to barrier insulators (DNA sequence)

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8
Q

DNA methylation is catalyzed by which enzymes

A

DNA methyltransferase enzymes (DNMT)

-occurs primarily in CpG dinucleotide

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9
Q

Northern blots are look ing at?

A

DNA

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10
Q

western blots are looking at?

A

protein

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11
Q

DNMTs have high affinity for… sites

A

hemimethylated sites which are heritable

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12
Q

Igf2 is … imprinted and it is en example of?

A

maternally imprinted

  • the ICR are not methylated, they will bind CTCF which is an enhancer blocking insulator
  • H19 gene is expressed
  • monoallelic inheritance
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13
Q

H19 is a … imprinted gene

A

-paternally
ICR DNA methhylation prevents CTCF binding, but tghe promotor foe H19 gets also methylated which prevents its transcription

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14
Q

dwarfism is due to….

A

the hypomethylation of the paternal allele aka Igf2 is not expressed

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15
Q

gigantism is due to…

A

hypermethylation of the ICR aka even the mom is methylated= more Igf2 and no H19

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16
Q

true or false: poky is cytoplasmicly inherited

A

true

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17
Q

what is heteroplasmy?

A

when there are 2 distinct mt populations in a single cell

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18
Q

what is homoplasmy

A

1 cell pop in a cell

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19
Q

factors influencing mitochondrial genome replication

A
  • Mitochondrial DNA is replicated within nucleoids
  • the nucleoids can divide within an organelle
  • Mitochondria themselves divide
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20
Q

why is the drosopjila development so fast?

A

because at the beginning fo their lives, the cell will divide as much as they can with the DNA provided by their moms

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21
Q

role of egg polarity genes and what are they?

A

make anterior and posterior in the boxy axis
they encode transcription factors
bicoid: anterior
nanos: posterior it inhibits the translation of the hunchback gene that is also provided by the mom

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22
Q

what are the roles of gap genes and what are they

A
  • they all encode for TFs
  • they are more for like thicc segments
  • hunchback is there too
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23
Q

Pair-rule genes:

A

-encode TFs
-each expressed in 7 stripes ex: eve
-it has to have more activators like hunchback, bicoid and less repressors like giant and kruppel in order to be expressed
-each enhancer jhas different arrangements of binding sites for maternally loaded factors and gap genes
-this allos enhancers to activate eve transcription in a specific stripe of nuclei
=combiinatorial control of transcription

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24
Q

what do segment polarity genes do?

A
  • encode components of 2 cell-cell signalling pathways: hedgehog ans wingless; included secreted proteins, membrane receptors and TFs
  • activated/repressed by oairule genes
  • make anterior and posterior in each segments, if one of them is messed up, they are all messed up
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25
Q

homeotic genes

A

identity of each segment is defines aka hox genes

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26
Q

drosophila embryogenesis:

A 
Egg polarity genes
gap genes
pair rule genes
segment polarity genes
homeotic genes
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27
Q

antigen

A

a molecule usually a protein that elicits an immune response

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28
Q

antibody:

A

proteins that binds to antigen marking them for destruction phy phagocytic cells

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29
Q

autoimmune diseases:

A

immune rection againts its own antigens

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30
Q

humoral immunity:

A

production and secretion of antibodies by B cells

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31
Q

cellular immunity:

A

T cells cproduce t cell receptors that recognize and bind antigens found on the surface of the bodys cells

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32
Q

why do vaccines work?

A
  • intact but inactivated pathogne
  • attenuated forms of the pathogen
  • purified components of the pathogen that have been found to be very immunogenic
  • vaccine then reduce the time it takes for the primary immune response so that when you have the second infection the body already have B cells ready
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33
Q

components of lights chains:

A
  • 2 types: kappa and lambda

- segments v,j and C

34
Q

components of heavy chains:

A
  • alpha delta, gamma. epsilon and mu

- segments V, D, J and C

35
Q

what are the 3 ways of generating diversity in B cells?

A
  • somatic recombination

- junctional diversity -somatic hypermutation

36
Q

somatic recombination:

A
  • between V and J segments
  • RAG1, RAG 2 and DNA repair enzymes introduce dsDNA breaks and joint random V and J segments
  • happens in the pre-mRNA to the mature mRNA
37
Q

true or false: VDJ segments contribute to antibody specificity

A

true

38
Q

Junctional diversity:

A

imprecise junction betweeen the segments

few random nuclotides are lost or gain= will usually produce nionfunctional gene

39
Q

somatic hypermutation:

A

usually between V gene segments

-deamination of cytosine which becomes uracil

40
Q

T cell receptor diversity

A
  • alpha chain: VJC segments
  • beta chain: VDJC
  • somatic recom and junction diversity but no somatic hypermutation
41
Q

silent mutations:

A

change the sequence but not the amino acid it encodes

42
Q

missence mutation:

A

change the sequence of a codon that encodes for a different amino acid

  • could be conservative aka the mutant codon encodes for a chemically similar amino acid
  • or non-conservative aka it encodes for a chemically different amino acid
43
Q

nonsense mutation:

A

change the sequence for a stop codon

44
Q

Frameshift mutation:

A

less revertants with ames test

  • caused by an insertion or deletion
  • change the translation reading frame for all codons
45
Q

hallmarks of cancer with proteins

A
  • sustaining proliferative signaling: RAS
  • evading growth suppressors: RB and P53
  • activating invasion and metastasis
  • enabling replicative immortality
  • inducing angiogesis
  • resisting cell death: P53
46
Q

what fucked up the 3T3 cells?

A

the src oncogene that transformed the normal cells to become insensitive to contact inhibition

47
Q

what causes breast cancer?

A

BRCA1 and 2

48
Q

what causes li-fraumenio syndrome?

A

p53

49
Q

what causes colon cnacer?

A

apc

50
Q

what causes retinoblastoma?

A

RB1

51
Q

true or false: oncogenes are dominant and usually arise from a single point mutation

A

true

52
Q

first oncogene:

A

c-src

53
Q

what are the 2 ways for a viral oncogene

A

1: retrovirus inserts its dna inthe cell which undergoes reverse transcription and inserts into the hosts chromosomes next to a protooncogene
- when the virus reprooduces, the proto-oncogene is incorporated in the virus
- repeated rounds of viral infection, the proto-oncogene becomes rearranged and mutated= producing an oncogene that is inserted back into the chromosome
- in v-src, the C term of the protein responsible for negative feedback becomes absent
2: retrovirus infects a cell and inserts near a proto-oncogene
- the strong viral promoter stimulated over-expression of the proto-oncogene

54
Q

in humams how do we usuallyu get cancer?

A
  • mutations

- innaproppropriate expression levels or forms

55
Q

what does the ras G12V do?

A

it makes it so that the ras is always in its GTP form and that it is always active so that at the end of the signaling, the map kinase will activate lots of TF and promote cellular growth

56
Q

chromosomal changes associated with cancer:

A
  • ch8 (can promote cell proliferation) and ch4 (promoter of immunoglobulin)
  • when there is a translocation aka the get together on the same strand of these 2, the product (protein)of ch4 is over expressed: proto-oncogene gets activated
  • same thing with ch9 and ch22. when there is trasnlovation, the protein has parts of the 2 chromosomes and it becomes an hyperactivated kinase
57
Q

hat is the drug that inhibits bcr-abl?

A

gleevec

58
Q

true or false; tumor suppressor mutations are dominant

A

false: they are recessive

59
Q

in which part of the cell cycle does RB play a role?

A

G1/s checkpoint

60
Q

what happens to the RB usually?

A

usually it is bound to E2F which is a transcription factor
-when there is accumulation of cyclin, it’ll phosphorylate the RB and it’ll detatch from the E2F and will get on a promoter and will stimulate gene replication

61
Q

what are the roles of p53?

A

-it can slow down cell proliferation until they are repaired or they can start senescence and do some apoptosis when the damage is too much

62
Q

role of p53 with Rb

A

usually p53 will make CDKN that stops cyclin production, so when p53 is mutated there is more cyclin aka more DNA replication

63
Q

why is RB inactivation good for virus?

A

because the inactivation willhelp the virus to be more expressed in the cells

  • hpv: E6 and 7 will block rb and p53
  • E1A and B will do the same in adeno virus
64
Q

True or false: cancer can only happen in like 2 steps when you have 2 mutations

A

falseeeee
ex: colon cancer it is a lot of mutations that happen over a long time and at the end you get cancer. You get mutations in p53, RB et etc

65
Q

New hallmarks:

A
  • deregulating cellular energetics
  • avoiding immune destruction
  • genome instability and mutation
  • tumor-promoting inflammation
66
Q

PD1: activation

A

the B 7 on the tumor is not the right one and so when the T cell get not activated by it then it’ll survive
-if the right ligant is on the tumor, then the T cell will die

67
Q

what blocks the major DNA

A

AMiNOPTERIN

68
Q

WHAT DI YOU NEET IN THE MINOR DNA PRECURSOR&

A

HPRT AND TK and you gro them in HAT medium

69
Q

how do you do cell fusion so that it works

A
  • we know that human chromosomes usually die in cell fusion
  • we mic a HPRT- human cell that has UMPK activity with a TK- monkey cell that does not have the UMPK activity and grow them in HAT medium
  • when the cell has HUMPK activity you are able to see what chromosomes are there and is able to know what human chromosomes are there
70
Q

what is gene therapy?

A

it involves adding normal copy if a gene to the genome of a mutated copy of a gene

71
Q

somatic cell gene therapy

A

transfer of a gene in somatic cells aka the patient will still transfer the defective gene to their kids

72
Q

germline gene therapy

A

the poerson will not transmit the defective gene to their kids

73
Q

Viral vectors:

A

1: derived to adenovirus:
will infect all cells even the nondividing ak amore stable ones
-the vectors will not be integrated in the genome, thus the transgene is diluted and eventually lost as all cells are dividing

2: most will infect only dividing cell but HIV will affect all without cell division
- the transgene and the viral vector will be incorporated into the genome

74
Q

types of gene therapy:

A

in vivo and ex vivo

75
Q

what is ADA-SCID

A
  • the T cells die ddue to no ada aka no immune system

- treatment: bone marrow transplantation

76
Q

construction of a vectpr:

A

_LTR is needed for the vector DNA integration in the cells

  • SV40 promoter will allow transgene expression in human cells
  • the neor is needed for the selection of human cells that will produce the virus in vitro
77
Q

issues with conventional gene therapy

A
  • Integration sites can’t be controlled
  • expression level of the rescue is not optimal
  • ex vivo experiment is limited top certain types of cells
  • solution: crispr
78
Q

transition vs transversion:

A
  • transition: purine to purine or pyrimidine to pyrimidine a-g or like c-t
    transversion: pyrimidine to purine or the other wat around: a to c or like G to T
79
Q

what is syneny?

A

the conserved order of genes between 2 genomes

80
Q

what is the role of the sigma factor

A

it is part of the RNA pol 2 and it recognizes and binds to the -10 and -35 regions where there are promoters. It positions the holoenzyme to correctly initiate transcription at the start site.

Biol 202 (2 decks)

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