Mat + Paternal genomes Flashcards

1
Q

how do embryos take control of their own development

A
  • first hours after fertilization, maternal factors in oocyte dictate early dvlpmnt. then zygotes genes take over
  • maternal to zygote transition needs epigenetic reprogramming (changes to chromatin structure, and resetting methylation on genome)
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2
Q

Explain the chromatin and methylation changes

A

C - chromatin in pronuclei take on open configuration then re-establishes local + global features

M - methyl marks removed. Paternal genome has rapid demethylation. Mat genome loses methylation passively after cell divisions

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3
Q

explain the transcirption changes and cell fate determination.

A

T - mRna in oocyte slowly depletes over 1st week dvlpmnt. But zygotic genome has multiple activations so genes expressed early for embryonic organisation + cell fate.

F - by 4-8 cell stage, some cells express genes causing them to become embryonic lineage (forms fetus) Other cells express genes linked with extraembryonic lineage (placenta)

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4
Q

what is parthenogenesis

A

** development without fertilisation (alternates with sexual repro)

some insects, haploid males develop from unfertilised eggs. Other parthenogenic organisms are diploid (oocyte genome replicated or Polar body not ejected.

  • they lack microtubule organiser.
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5
Q

Brief explain parthenogenesis in mouse (pic pg 7)

A

. If polar body not ejected, egg is diploid.
. But the parth fatuus is too small + placenta abnormal. (so degenerates till mid pregnancy)
. this happens too if foetus develops from zygote with 2 F pronuclei
. If zygote 2 M pronuclei, placenta big enough but foetus more underdeveloped.

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6
Q

what is genomic imprinting and where does it occur

A

related to diff methylation of maternal / paternal genes in mammals.
In humans 9 chromosomes known to hv regions of genes that are imprinted.

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7
Q

Briefly explain what genomic imprinting involves

A

> During meiosis methylation of Mat +Pat DNA equal. then ovaries all chromosomes methylated as maternal, testes paternal.

> Some imprinted gens, only 1 copy (m or P) of same gene need be active.
Error in imprinting may mean gene that is tuned off when shud be on (vice versa)
Result = activation of both genes/ blocking of them

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8
Q

What is Prader Willi + Angelman syndrome. what causes it

A

PW - only maternal genes expressed
A - only paternal genes expressed

  • defect = small section of chromosome 15 is missing/partially expressed
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9
Q

what is chorioandenoma (abnormal fertilisation)

A

. type of uterine cancer, tumour origin = growing placenta without foetus.
. usually when a zygote doesn’t hv female pronucleus with diploid male.
CAN SPREAD TO OTHER PARTS - also called invasive hyatidiform mole

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10
Q

Give the 2 mechanisms to develop uniparental chorioadenoma

A

> oocyte without viable chromatin fuses with 1 spermatazoon, male pronucleus then does replication

> oocyte without viable chromatin fuses with 2 spermatozoa, then 2 male pronuclei fuse + forms diploid nucleus.
** tumour tissue = pat genome (androgenic hydatidiform mole)

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11
Q

how does Biparental chorioadenoma form

A

gene mutations that totally disturb imprinting mechanisms in embryo,

> maternally imprinted genes BLOCKED
paternally imprinted genes OVEREXPRESSED

  • result = trophoblast (cells that normally turn into placenta) is overdeveloped, therefore foetus not developed.
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