lecture 21 Flashcards
(25 cards)
what is the starting point of PEV mutations?
what is E var?
what is Su var?
1) mutated white due to an inversion placing it close to heterochromatin causing it to spread with a little bit of red spots
2) makes euchromatin, which allows for more white pigment to expand–> these are enhancer sequences
3) makes heterochromatin–>restricts the spread of white heterochromatin–> this is a repressor and increases the extent of normal pigment
what are some Su Var mutations caused by?
what do Su(var) mutations also affect?
loss of function HP1—> interferes with heterochromatin formation
affects HMTs’—> H3k9 is not properly methylated, epigenetic methylation is not established and heterochromatin formation is inhibited
both TrxG and PcG protein complexes are recruited to _____ sequences by _______ DNA binding factors
what does the poly comb group (PcG) do and how?
what do trithorax (TrxG) do and how?
specific DNA sequences by DNA binding factors (activators and repressors)
repress gene expresssion by recruiting histone modifying complexes that deacetylate histones
activated gene expression by recruiting complexes to acetylate histones
what happens when thrithorax complex is mutate?
what happens when the poly comb complex is mutated?
no active boundaries will spread–> inactivating the wild type pigment gene
move boundary & less htererochromatin will spread, wild type is more transcribed
what are epigenetic patterns heritable thru in somatic cells?
how is it maintained in somatic cells?
mitosis from generation of cells to the next–> parent to sibling
–acteyl + methyl nations present on the histones before DNA replication must be maintained or established on both the old and new histones after replication
the formation of germ cells must ?
clear replicating chromatin of the majority of accumulated epigenetic marks
so marks added are erased during meiosis
which gene is from the dad and from the mom and what do they do?
what chromosome r they on?
parental: IGF2—-> pro growth , silenced on mom
maternal: H19–> tumor suppressor gene, silenced on dad
chromosome 11
how are H19 and IGF2 inherited?
in primordial germ line cells, the inherited patters are first erased & then reestablished in sex specific pattern of the germ line in early gametogenesis
how does mitotic methylation pattern being passed on work?
what is maintenance methylation?
before replication, both are methylated
after–> each sister chromatid has methylated and non methylated strand
DNA methyltransferase recognizes semi methylated DNA and methylates the other strand
if a gene is not imprinted, where is it inherited from ?
what if it is imprinted?
inheriting mutations from both will have the SAME affect
alleles of the imprinted genes are inactive from one parent and active in another parent
what are ways to store info within cells? what is stable to transcient?
DNA seq– transgenerational –> most stable
DNA methyl
histones
gene regulatory networks
physiological state —> transient
what are the 2 definition of epigenetic?
gene activity 1 can have a stimulus that acts on chromatin and modifies in–> leading to change on gene 2 activity
there can be a stimulus that acts on gene 1–> which is maintained thru chromatin modifications–> leading to activity change in gene 1
how does variegation work?
what is methylated?
what is the affect of H3 lysine 9 histone methlyltransferase?
there is an inversion, which displaces the red gene and makes it be repressed because heterochromatin spread
Hp1
H3K9me
stops spreading of heterchromatin so will not spread at much–> will have more red!
what is the PEV organism, affect, heritability, mechanism, and importance?
drospholia
pigment in eye cells
mitotic only
histone mods
aftirical
what is turner and Klinefletr syndrome?
turner– no inactive z in females—XO
XXY– one inactive X
how do X inactivating mechanisms work?
if more than one X, one is inactivated randomly in the embryo then it keeps dividing –> it is epientically inherited
what is the n-2 rule?
all Xs in excess of one will be inactive in females
xx–> Xi +Xa
XXY–> Xi+Xa
what is the organism, affects, heritability, inhereatance mechanism and importance of X inactivation?
many
dosage of X chromosomes
mitotic only
histone mods
essentral for proper gene expression from X
how are imprints erased and reestablished?
exist in the zygote then in somatic cells
when somatic turn into a germline F or M, imprints are erased–> then are established
what does the maternal gene have that does not allow it to express IGF2?
what doe the paternal have that allows for IGF2 expression?
has insulator element after the IGF2 gene –> blocks looping of enchancer and IGF2
so H19 is after the insulator and binds the enhancer–>transcription
the insulator after IGF2 is methylated, along with H19
this allows for looping of enhancer to IGF2
what is the organism, what does it affect, what is the heritability and what is the inheritance and importance of imprinting?
mammals
maternal/paternal alleles
mitotic only
DNA methylaiton
proper embryonic development
when is the FLC gene on / off?
what is FLC?
plants don’t flower in the fall
FALL– FLC is on
winter– FLC off
spring–flc off
summer–FLc off
flower repressor
what does always vernalized , normal response, and never vernatlized show?
always: FLC never active –> euchromatin
normal: repressed by cold–> FLC off
never: FLC active–> repressed –> hetercrhoamtin
what is the organism, affects, heritability, inheritance mechanisms, importance?
plants
FLC expression
mitotic
histone mods
prevent fall flowering
