Embryonic senescence and laminopathies in a progeroid zebrafish model.

ABSTRACT:

Background

Mutations that disrupt the conversion of prelamin A to mature lamin A cause the rare genetic disorder Hutchinson-Gilford progeria syndrome and a group of laminopathies. Our understanding of how A-type lamins function in vivo during early vertebrate development through aging remains limited, and would benefit from a suitable experimental model. The zebrafish has proven to be a tractable model organism for studying both development and aging at the molecular genetic level. Zebrafish show an array of senescence symptoms resembling those in humans, which can be targeted to specific aging pathways conserved in vertebrates. However, no zebrafish models bearing human premature senescence currently exist.

Principal findings

We describe the induction of embryonic senescenc

SUBMITTER: Koshimizu E 

PROVIDER: S-EPMC3068137 | biostudies-literature | 2011 Mar

REPOSITORIES: biostudies-literature