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Epigenetics: Histone Modification II

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Presentation on theme: "Epigenetics: Histone Modification II"— Presentation transcript:

1 Epigenetics: Histone Modification II

2 trithorax-Group (trxG)
Maintain the “on” state of developmental regulatory genes trx: founding member (HMT on H3K4)

3 Transcriptional memory by trxG and PcG
trxG – on state memory PcG – off state memory

4 Regulation of Hox by trxG and PcG
segmentation genes establish 14 segments Hox genes maintain the identity of these segments trxG and PcG control Hox defects in trxG or PcG cause hometic mutatios

5 Other examples of trxG phenotypes
a vs b : wild type and trx mut c : balancer into small wing d : fifth seg mimicking anterior seg

6 Identification Strategy for trxG genes reversal for PcG mutants
trxG mutants as suppressor of PcG mutants reversal of Polycomb phenotype in double mutants opposite outcome on same pathways activator vs repressor on Hox gene

7 Two major groups of trxG
Group 1: ATP-dependent chromatin remodeling complexes (SWI2/SNF2, Brahma, BRG1) Group 2: HMTs on H3K4 (Set1, MLL1, MLL2)

8 ATP-dep chromatin remodeling complexes
Bromo-domain: recognize Acetylated Histone Many complexes are equipped with Both readers (bromo-domain) and writers (Histone Acetyl Transferase) -> maintaining active “ON” state

9 Modes of chromatin remodeling

10 Genome-wide distributions of trxG
A) BRM complex: more global roles In general transcription control B) TRX: less limited number of loci

11 Inter-dependence of trxG and PcG
PcG-dep repression is a default state trxG-dep activation an anti-repression to PcG share targeting proteins between trxG and PcG: Zeste and GAGA factor mechanistically feasible: H3K4me3 -> HAT -> Acetylation on H3K9 or H3K27 -> block methylation on H3K9 or H3K27


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