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Vertebrate development > Genomic imprinting > Flashcards

Genomic imprinting Flashcards

1
Q

Examples of:
Writers/Initiators

Maintainers

Readers

Erasers

A

Dnmt3
lncRNa
Histone methyltransferases

Dnmt1

DNA methylation binding proteins
TFs

Deacetylases
Demethylases

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2
Q

Epigenome functions

A

Maintains DNA integrity in cell cycle

Regulates gene expression

Responds to internal + external enviros

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3
Q

Epigenetic therapy
e.g. in cancer

  • targets
  • effects
A

DNMT inhibitors
HDAC inhibitors

TSG expression
Apoptosis
Immunomodulation

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4
Q

Nucelar transfer
- Gynogenetic

  • Androgenetic
A

Replace male pronucleus w/ female one
= (2 female nuclei)

Replace female pronucleus w/ male one

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5
Q

What happens in an oocyte doesn’t exclude the 2nd polar body?

A

Activates 2nd polar body

= Parthenogenetic

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6
Q

Why do we need 2 parental genomes for normal development?

A

2 female pronuclei
= hardly any extra embryonic tissue
- tiny embryo that doesn’t develop
(no placental support)

2 male pronuclei
= lots of ExEmbryonic tissue
- hardly any embryo

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7
Q

Prader-Willi syndrome

A

Uniparental disomy of 15q11-q13

Deletion of paternal copy

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8
Q

Angelman syndrome

A

Uniparental disomy of 15q11-q13

Deletion of maternal copy

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9
Q

Genomic imprinting

- define

A

Subset of genes epigenetically silenced on 1 parental allele during germ-line development

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10
Q

Genomic imprinting

- is it maintained?

A

Silencing maintained throughout development

Reset in germ-line of next gen.
= a transgenerational epigenetic phenomenon

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11
Q

Theories for why genomic imprinting occurs

A

> genetic conflict
- competition of genomes for maternal resources

> dosage compensation

> placental development

> prevention of parthenogenesis

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12
Q

Haig parental conflict hypothesis

AKA Kinship theory

A

Mothers know offspring is their’s
Males need to compete w/ other to get genes into next gen.

Mother doesn’t invest all resources into 1st pregnancy
- going to have more

Males don’t know if a child is theirs so need to compete for resources
- want their offspring to outcompete other genomes

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13
Q

Haig parental conflict

- female vs. male characteristics

A

Female:
Growth suppressing
Preservation of maternal resources
TSGS

Male:
Growth promoting
Competition of His offspring for maternal resources
Oncogenes

Selfish gene concept
= purpose of life is to get YOUR genome into the next gen.

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14
Q

Imprinted genes

- monogamous species

A

Fewer imprinted genes as less reason to compete

However never always some cheating as never 100% monogamous

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15
Q

What happens when you cross a monogamous x polyandrous species ?

A

= imprinting defects

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16
Q

Coadaptation theory

A

Imprinted genes act co-adaptively to optimise foetal development
+ maternal provisioning + nurturing

17
Q

Maternal provisioning

A

Size + energy content of eggs

18
Q

Coadaptation

- e.g. Peg3

A

Subset of mainly paternally expressed genes expressed in placenta + hypothalamus of brain

If no Peg3

  • > mother has no maternal instinct
  • > leaves offspring
19
Q

Imprinted genes

- genome organisation

A

MEGs + PEGs clustered

- assume they work together in a network

20
Q

Primary hallmarks of imprinting

- DNA methylation

A

Methylated = inactive
- TFs can’t bind to closed chromatin

Demethylated
= active

21
Q

DMR

AKA imprinting control regions

A

Differentially methylated regions

- different methylation status across samples

22
Q

Primordial germ cells

- DNA methylation

A

Methylation imprints erased + re-established

Genital marks added when cells are at genital ridge

23
Q

Embryonic reprogramming

- occurs in 2 major development phases

A
  1. in PGCs
    - global demethylation
    - > then remethylation
    - > in fertilisation active demethylation of male pronucleus, slow demethylation of female pronucleus
  2. Imprinted genes resistant after fertilisation
24
Q

Promoter methylation model

A

Methylated promoter
= silenced allele

Unmethylated
= active allele

25
Q

lncRNA model

A

antisense methylation stops the lncRNA from silencing adjacent genes

-> prevents 2 polymerases clashing
(would prevent transcription)

26
Q

Boundary model

A

CTCF (zinc finger-like protein) binding site produces a boundary between 2 genes

  • separates genes into 2 domains
  • > 1 active, 1 silenced

CTCF can only bind to a demethylated DMR

2 genes unaffected by each other

27
Q

Prader Willi syndrome

A

Hypotonia - weak m

28
Q

Prader Willi syndrome

A

Hypotonia - weak muscle tone

Hypogonadism - immature development of sexual organs

CNS dysfunction

29
Q

Angelman syndrome

A

Speech impairment

Balance disorder

Unique behaviours

30
Q

Functions of imprinted genes

A

Foetal growth regulation

Regulate metabolism
e.g. Peg3 in hypothalamus

Regulate behaviour
e.g. Peg3 milk release (mother) + suckling (newborn)

Vertebrate development (12 decks)

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