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- The Notion of Epigenetics
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1. Cytoplasmic epigenetics: inheritance by cytoplasmic continuity
- Prof. Philippe Silar
- Dr. Fabienne Malagnac
- Epigenetics: Paradigms
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2. The molecular mechanism of X chromosome inactivation
- Prof. Neil Brockdorff
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3. Genomic imprinting: history and embryology
- Prof. Davor Solter
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4. X chromosome inactivation in human cells
- Prof. Barbara Migeon
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5. RNAi and heterochromatin in plants and fission yeast
- Prof. Robert Martienssen
- Epigenetics: Mechanisms
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6. Polycomb epigenetic mechanisms: role of PcG complexes
- Prof. Vincenzo Pirrotta
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7. Polycomb epigenetic mechanisms: methylation of DNA
- Prof. Vincenzo Pirrotta
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8. Histone modifications and prospects for an epigenetic code
- Prof. Bryan Turner
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9. Epigenetic control by histone methylation
- Prof. Thomas Jenuwein
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10. Histone dynamics, heritability and variants
- Dr. Genevieve Almouzni
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11. Gene silencing in budding yeast
- Prof. Susan Gasser
- Epigenetics: Heritability and Reversibility
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12. Nuclear cloning, stem cells and epigenetic reprogramming
- Prof. Rudolf Jaenisch
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13. Stem cell memory
- Prof. James Sherley
- Archived Lectures *These may not cover the latest advances in the field
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14. Epigenetics: a historical overview
- Dr. Robin Holliday
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15. DNA methylation
- Prof. Adrian Bird
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16. DNA methylation and genome defense in Neurospora crassa
- Prof. Eric Selker
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18. Evolution of mammal epigenetic control systems
- Prof. Jenny Graves
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19. Genomic imprinting and its regulation
- Dr. Anne Ferguson-Smith
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20. Nuclear organization and gene expression
- Prof. David Spector
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21. Germ cells
- Prof. Azim Surani
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22. Epigenetic regulation of phenotype
- Prof. Emma Whitelaw
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24. Cytoplasmic epigenetics: proteins acting as genes
- Prof. Reed Wickner
Printable Handouts
Navigable Slide Index
- Introduction
- Dynamic activities of PcG complexes
- PRC2 has also an untargeted global function
- Chromatin immunoprecipitation (ChIP-seq) profiles
- Remethylation after DNA replication (1)
- Remethylation after DNA replication (2)
- Directing and maintaining H3K27 methylation
- What happens if remethylation is prevented?
- 3 complexes with antagonistic activities
- The CBP/p300 acetylase complex
- The TRR complex (MLL3,4 in mammals)
- The DNA accessibility model (1)
- The DNA accessibility model (2)
- Even repressors require access to DNA
- Global H3K27me2 acts as a regulator
- How do PcG complexes repress? (1)
- How do PcG complexes repress? (2)
- The bright red eye color requires the white gene
- Adding a PRE to the transgene
- PcG complexes enhances repression locally
- Pairing-sensitive silencing
- Pairing-dependent silencing
- PcG targets tend to associate in the nucleus
- PcG complexes in the nucleus
- Do PcG proteins prevent promoter access? (1)
- Do PcG proteins prevent promoter access? (2)
- Does H2AK119ub interfere with transcription?
- Complete loss of H2AK119ub (1)
- Complete loss of H2AK119ub (2)
- H3K27 methylation
- The essential role of canonical PRC1
- Links between PRC1 and PRC2
- Active and repressed chromatin marks
- The bivalent state
- Bivalency resolved
- Not so simple
- Bivalent domains in nucleosomes
- DNA methylation: understanding bivalency
- Relationship to DNA methylation (1)
- Relationship to DNA methylation (2)
- Relationship to DNA methylation (3)
- The role of the bivalent state
- Enormous progress has been made
- Thank you
Topics Covered
- PRC2 has an untargeted global function
- Chromatin immunoprecipitation (ChIP-seq) profiles
- H3K27 methylation
- The CBP/p300 acetylase complex
- The TRR complex (MLL3,4 in mammals)
- The DNA accessibility model
- How do PcG complexes repress?
- The essential role of canonical PRC1
- Links between PRC1 and PRC2
- The bivalent state
Talk Citation
Pirrotta, V. (2017, December 31). Polycomb epigenetic mechanisms: methylation of DNA [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 26, 2024, from https://doi.org/10.69645/BGFY9197.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Vincenzo Pirrotta has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
A selection of talks on Cell Biology
Transcript
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0:00
Hello. My name is Vincenzo Pirrotta,
and this is part two of our talk about Polycomb Epigenetic Mechanisms.
0:09
As we have seen,
a more useful way to look at polycomb group activities,
is to think of them as involved in dynamic processes.
And in particular, a polycomb complex like PRC2.
PRC2 target all chromatin,
not just polycomb group target sites,
where it is found stably bound.
0:30
PRC2 in fact has clearly untargeted functions.
If we look at histone H3 methylation at lysine 27 in the whole genome.
It is clear that most of the activity of PRC2 is not to
trimethylate but to dimethylate lysine 27 of histone H3.
It appears that PRC2 acts on most of the nucleosomes in the genome.
There is only a small percentage of histone H3 that remains unmethylated and note that
a small amount at any one time is acetylated at lysine
27 and therefore cannot be methylated at that position.
1:11
Chromatin immunoprecipitation and sequencing, so ChIP-seq,
so-called allows us to map where these different states have methylation
are in the genome relative to the genes and the activity of these genes.
The sites where polycomb protein is bound representing
PRC1 or polycomb target genes are also regions that contain histone H3 trimethylation.
Instead, dimethylation of lysine 27 is found almost everywhere,
particularly in genomic regions that are not transcriptionally active,
intergenic regions or genes that are weakly or not at all transcribed.
So this is in fact, most of the genome.
Monomethylation of lysine 27 is found at
actively transcribed genes which are indicated
here by the presence of RNA polymerase, Pol II.
And monomethylation is probably an intermediate of dimethylation or remethylation.