학술논문

A Reconfigured Pattern of MLL Occupancy within Mitotic Chromatin Promotes Rapid Transcriptional Reactivation Following Mitotic Exit
Document Type
Report
Source
Molecular Cell. Dec 24, 2009, Vol. 36 Issue 6, p970, 14 p.
Subject
Genetic research -- Genetic aspects
Genetic research -- Analysis
Genomics -- Genetic aspects
Genomics -- Analysis
Chromatin -- Genetic aspects
Chromatin -- Analysis
Gene expression -- Genetic aspects
Gene expression -- Analysis
Anopheles -- Genetic aspects
Anopheles -- Analysis
Enzymes -- Genetic aspects
Enzymes -- Analysis
Leukemia -- Genetic aspects
Leukemia -- Analysis
Methylation -- Genetic aspects
Methylation -- Analysis
Language
English
ISSN
1097-2765
Abstract
To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.molcel.2009.12.001 Byline: Gerd A. Blobel (2), Stephan Kadauke (2), Eric Wang (1), Alan W. Lau (3), Johannes Zuber (1), Margaret M. Chou (3), Christopher R. Vakoc (1) Keywords: DNA; CELLCYCLE Abstract: Mixed lineage leukemia (MLL) and its metazoan Trithorax orthologs have been linked with the epigenetic maintenance of transcriptional activity. To identify mechanisms by which MLL perpetuates active transcription in dividing cells, we investigated its role during M phase of the cell cycle. Unlike other chromatin-modifying enzymes examined, we found that MLL associates with gene promoters packaged within condensed mitotic chromosomes. Genome-wide location analysis identified a globally rearranged pattern of MLL occupancy during mitosis in a manner favoring genes that were highly transcribed during interphase. Knockdown experiments revealed that MLL retention at gene promoters during mitosis accelerates transcription reactivation following mitotic exit. MLL tethers Menin, RbBP5, and ASH2L to its occupied sites during mitosis, but is dispensable for preserving histone H3K4 methylation. These findings implicate mitotic bookmarking as a component of Trithorax-based gene regulation, which may facilitate inheritance of active gene expression states during cell division. Author Affiliation: (1) Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA (2) The Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA (3) University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA Article History: Received 8 April 2009; Revised 3 August 2009; Accepted 3 December 2009 Article Note: (miscellaneous) Published: December 24, 2009