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Genetics > Epigenetics > Flashcards

Epigenetics Flashcards

1
Q

change in an expression of genes that changes the phenotype without changing the DNA

A

epigenetics

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2
Q

what does epigenetics change then

A

chromatin structure

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3
Q

are epigenetics passed on to the next generation or through cell division

A

yeah they are heritable

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4
Q

two types of chromosome

A

euchromatin and heterochromatin

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5
Q

which type of chromosome is transcriptionally active and decondensed?

A

euchromatin

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6
Q

which type of chromosome is transcriptionally inactive and condensed

A

heterochromatin

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7
Q

enzyme used for methylation

A

DNA methyltransferase enzyme

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8
Q

where is the methyl group added in methylation of cytosine

A

5’ carbon to make 5’ methyl cytosine

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9
Q

which one of the enzymes methylates unmethylated DNA

A

Dnmt3 (DNA methyltransferase)

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10
Q

what enzymes/process occurs when you have a completed methylated DNA

A

MeCP2 binds to they methylated DNA

then recruits HDAC1/2 (and mSin3A) which deacetylases the histones

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11
Q

what is the point of deacetylasing the histone

A

it makes the histone more positive so that it will be more attracted to the negative DNA hence forming a heterochromatin

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12
Q

what happens to the methylated DNA after cell division

A

it becomes a hemimethylated DNA where one strand is methylated and the other isn’t

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13
Q

what happens to the hemimethylated DNA

A

MeCP2 binds to it (allosteric property allows it to change shape based on what it is bound to)

MeCP2 then recruits Dnmt1 to methylate the other strand of DNA so now you have 2 completely methylated DNA strands

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14
Q

what happens to the DNA after Dnmt1 has been recruited to methylate the unmethylated strands

A

MeCP2 then goes through a conformational change which now it recruits HDAC1/2 (and mSin3A) to deacetylase the histone so it is positive making it more attracted to DNA to form heterochromatin

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15
Q

enzymes used for deacteylasing histone and for acetylasing histone

A

deacetylasing - HDAC (more positive)

acetylasing - HAT (more neutral)

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16
Q

when does switching of globin chains of hemoglobin occur

A

fetal development of human

6 weeks - E globin is active and 12 weeks gamma globin is active

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17
Q

what regulates the switching of globin in humans

A

changes in DNA methylation of control regions in the promoter of the genes encoding the different forms of globin protein

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18
Q

Immunodeficiency-centromeric instability-facial anomalies syndrome aka ICF is caused by a mutation of what

A

Dnmt3b gene

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19
Q

facial dysmorphism, mental retardation, recurrent and prolonged infections, and variable immune deficiency with a constant decrease of IgA are symptoms of what

A

mutation in Dnmt3b gene

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20
Q

inheritance of ICF

A

rare autosomal recessive

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21
Q

ICF leads to instability in which chromosomes

A

1, 9, and 16

22
Q

why is Rett syndrome rarely occur in boys

A

it is lethal in vitro - only ones that survive are those that have Klinefelters because they have two X alleles (46XXY)

23
Q

at what point do children with retts start to regress in development

A

6 - 18 months

24
Q

Rett is a mutation in what

A

MeCP 2 (methyl cytosine bind protein 2)

25
Q

mono allelic expression due to

A

genomic imprinting

26
Q

DNA methylation marks a gene for

A

epigenetic repression and genomic imprinting

27
Q

genomic imprinting goes against what law

A

Gregor Mendel’s law of biallelic expression that equal genetic contribution to offspring made by each parent

28
Q

if you are maternally imprinted, what does that mean

A

copy you get from mom is shut off

29
Q

how does genetic imprinting mess with the pedigree

A

can’t tell if disorder is recessive or dominant (based on which parent is imprinted or not)

30
Q

when does imprinting occur

A

gametogenesis

31
Q

voracious appetite (elevated ghrelin), food hoarding and other OCD behavior, skin picking, sleep disturbance/sleep apnea, short stature, hypopigmentation, hypofunctioning of the hypothalamus are all symptoms of

A

Prader Willi

32
Q

Prader Willi and Angelman are chromosomal deletion in what chromosome

A

15

33
Q

in Angelman, persons has two copies of?

A

SNRPN

34
Q

in Prader Willi, persons has two copies of

A

UBE3A

35
Q

population that has a higher chance of having Beckwith Wiedemann syndrome

A

persons of in vitro fertilization (1 in 4000)

36
Q

abnormal DNA methylation of what region in Beckwith Wiedemann

A

11p15

37
Q

child has two copies of whose genes in Beckwith

A

paternal disomy

38
Q
  • macroglossia (enlarged tongue)
  • birth weight and length greater than 90 percentile -abdominal wall defects such as umbilical hernia -ear creases or pits
  • neonatal hypoglycemia
  • increased risk of cancer
A

Beckwithe

39
Q

how does methylated DNA show up on electrophoresis

A

it would be a heterochromatin so would not be cut by restriction enzymes hence are so big and would not travel that far from point of origin

40
Q

treatment drugs for abnormal methylation

A

interfere with DNA methylation (5 aza cytidine ) and histone deacetylation (sodium butyrate)

41
Q

genes that have been shown to be abnormally methylated

A

IGF2 (insulin like growth factor) and IGF2 receptors

42
Q

Environmental Factors that have been show to influence or disrupt epigenetic gene silencing

A

temperature, toxins, maternal care, diet, hypoxia

43
Q

glucocorticoid receptor level in healthy individuals

A

high (so not methylated)

44
Q

effects of high glucocorticoid receptors

A

individual can handle stress better

45
Q

during pregnancy, environmental exposure affects which generation

A

1st, 2nd, 3rd, and sometimes even 4th

because women are born with all their eggs (and not making any more)

46
Q

when are effects of environmental exposure the most pronounced

A

during reproductive stem cell differentiation

47
Q

what does epigenetic glucose sensing switch cause

A

DNA hypomethylation and histone acetylation —-> expression of orexin

48
Q

what does orexin producing neurons do

A

regulate feeding behavior, lipid metabolism, sleep/wakefulness

49
Q

HBP (hexosa-mine biosynthesis pathway) integrates the metabolism of what

A

glucose, glutamine, acetyl CoA and uridine disphosphate into UDP-GlcNac

50
Q

UDP-GlcNac is metabolized to

A

sialic acid, N-acetyl- neuraminic acid (Neu5Ac) through intermediate ManNac

51
Q

X inactivation occurs by?

A

DNA methylation and epigenetics

52
Q

incontinentia pigmenti is a mutation of

A

X-linked IKBKG gene

Genetics (19 decks)

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