QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

First published online October 10, 2008
doi: 10.1242/10.1242/dev.000844

This Article Summary Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Dominguez, M. Articles by Berger, F. Search for Related Content PubMed PubMed Citation Articles by Dominguez, M. Articles by Berger, F. Social Bookmarking                         What's this?

Chromatin and the cell cycle meet in Madrid

¹ Instituto de Neurociencias, CSIC-UMH Unidad de Neurobiología del Desarrollo, Campus de Sant Joan, Apto 18, 03550 Sant Joan d'Alacant, Alicante, Spain.
² Temasek Life Sciences Laboratory, 1 Research link, National University of Singapore, 117604 Singapore.

View larger version (19K): [in this window] [in a new window]   Fig. 1. Known and hypothetical controls linking the cell cycle and chromatin modification. The controls of the G1-S phase transition of the cell cycle (blue circles) regulate DNA methylation and histone modifications (dark-purple hexagons), which also regulate eachother. Nucleosome assembly (green) onto newly replicated DNA at the replication fork is depicted. DNA methylation (light-purple hexagon) is replicated in a semi-conservative manner. Whether histone modifications are transmitted through cell division in a semi-conservative manner remains a matter of debate. During the S phase, replication-coupled histone replacement (orange box) is likely to play a role in chromatin dynamics. The G2-M transition is also correlated with histone modifications. During the G2 and G1 phases, non-replicative histone replacement (orange box) might play a role in chromatin dynamics, which could be important for the decision whether to enter a new replication cycle or to differentiate.

View larger version (13K): [in this window] [in a new window]   Fig. 2. Chromatin control of cell proliferation and reprogramming. (A) PRC1 and PRC2 complexes help to maintain cells in an uncommitted, mitotically active stem-like state by silencing differentiation genes. Polycomb group (PcG) proteins are found in two main Polycomb repressive complexes (PRCs), the initiating complex PRC2 (red) and the maintenance complex PRC1 (green), but other PRC complexes have also been detected or predicted (purple, see B). PRC2 members Extra sexcombs (Esc)/EED (yellow oval) and E(z)/EZH2 (orange oval) methylate (blue hexagons) histone H3 at lysine 27 (arrow), and this epigenetic mark is recognized and bound by the chromodomain-containing protein Pc/HPC (green oval), a component of PRC1, to form stable, repressive chromatin. (B) Other forms of PRC (purple) have been detected and may instead repress cell proliferation and favor differentiation. The dynamic formation of distinct isoforms of PRC complexes may help to define the dynamic reprogramming of the genome at the transition from proliferation to differentiation. How PRC2 and PRC1 are recruited to specific genes remains poorly understood.

CiteULike

Complore

Connotea

Del.icio.us

Digg

Reddit

Technorati

Twitter