English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Knockout mice provide novel insights into meiotic chromosome and telomere dynamics

MPS-Authors
/persons/resource/persons50515

Scherthan,  Harry
Dept. of Human Molecular Genetics (Head: Hans-Hilger Ropers), Max Planck Institute for Molecular Genetics, Max Planck Society;

External Resource
No external resources are shared
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

Scherthan, H. (2003). Knockout mice provide novel insights into meiotic chromosome and telomere dynamics. Cytogenetic and Genome Research, 103(3-4), 235-244. doi:10.1159/000076809.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0010-8B0D-E
Abstract
Meiosis is a succession of two specialized cell divisions that leads to the formation of gametes and thereby compensates for genome doubling at fertilization. During the extended prophase of the first meiotic division chromosomes assemble protein cores (axial elements) that attach their ends to the nuclear envelope. These ends transiently gather at a limited sector of the nuclear periphery (bouquet stage) at a time when meiotic recombination is initiated and when chromosomes initiate stable pairing (synapsis). This review discusses novel insights into the relation between recombinational DNA repair and meiotic telomere dynamics that have arrived from recent studies of transchromosomal mice and knockout mice. Analysis of mice deficient for A-type lamins, histone H2AX, Suv39h HMTases, and the AE protein SYCP3 suggests that entry into prophase I requires heterochromatin integrity and lamin A expression. Initiation of meiotic telomere clustering represents an early recombination-independent event in first meiotic prophase, while exit from the bouquet stage depends on signals that emanate from the progress of recombinational DNA repair as sensed by ATM kinase and relayed through histone H2AX.