1097-4652/asset/JCP_left.gif?v=1&s=55bd21dc6c29ea5f5b29e4649eaeb334c7805008)
Original Article
Mutation of the SNF2 family member Chd2 affects mouse development and survival
Article first published online: 29 JUN 2006
DOI: 10.1002/jcp.20718
Copyright © 2006 Wiley-Liss, Inc.
Additional Information
How to Cite
Marfella, C. G., Ohkawa, Y., Coles, A. H., Garlick, D. S., Jones, S. N. and Imbalzano, A. N. (2006), Mutation of the SNF2 family member Chd2 affects mouse development and survival. Journal of Cellular Physiology, 209: 162–171. doi: 10.1002/jcp.20718
Publication History
- Issue published online: 26 JUL 2006
- Article first published online: 29 JUN 2006
- Manuscript Accepted: 5 JUN 2006
- Manuscript Received: 14 APR 2006
Funded by
- National Cancer Institute. Grant Number: CA95216
- UMMS Diabetes Endocrinology Research Center. Grant Number: DK32520
- Abstract
- Article
- References
- Cited By
Abstract
The chromodomain helicase DNA-binding domain (Chd) proteins belong to the SNF2-like family of ATPases that function in chromatin remodeling and assembly. These proteins are characterized by the presence of tandem chromodomains and are further subdivided based on the presence or absence of additional structural motifs. The Chd1–Chd2 subfamily is distinguished by the presence of a DNA-binding domain that recognizes AT-rich sequence. Currently, there are no reports addressing the function of the Chd2 family member. Embryonic stem cells containing a retroviral gene-trap inserted at the Chd2 locus were utilized to generate mice expressing a Chd2 protein lacking the DNA-binding domain. This mutation in Chd2 resulted in a general growth delay in homozygous mutants late in embryogenesis and in perinatal lethality. Animals heterozygous for the mutation showed decreased neonatal viability and increased susceptibility to non-neoplastic lesions affecting most primary organs. In particular, approximately 85% of the heterozygotes showed gross kidney abnormalities. Our results demonstrate that mutation of Chd2 dramatically affects mammalian development and long-term survival. J. Cell. Physiol. 209: 162–171, 2006. © 2006 Wiley-Liss, Inc.