Mat + Paternal genomes Flashcards
how do embryos take control of their own development
- 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)
Explain the chromatin and methylation changes
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
explain the transcirption changes and cell fate determination.
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)
what is parthenogenesis
** 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.
Brief explain parthenogenesis in mouse (pic pg 7)
. 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.
what is genomic imprinting and where does it occur
related to diff methylation of maternal / paternal genes in mammals.
In humans 9 chromosomes known to hv regions of genes that are imprinted.
Briefly explain what genomic imprinting involves
> 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
What is Prader Willi + Angelman syndrome. what causes it
PW - only maternal genes expressed
A - only paternal genes expressed
- defect = small section of chromosome 15 is missing/partially expressed
what is chorioandenoma (abnormal fertilisation)
. 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
Give the 2 mechanisms to develop uniparental chorioadenoma
> 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)
how does Biparental chorioadenoma form
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.