Lamin B1 and lamin B2 are long-lived proteins with distinct functions in retinal development

David Razafsky, Candace Ward, Chloe Potter, Wanqiu Zhu, Yunlu Xue, Vladimir J. Kefalov, Loren G. Fong, Stephen G. Young, Didier Hodzic

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

Abstract

Lamin B1 and lamin B2 are essential building blocks of the nuclear lamina, a filamentous meshwork lining the nucleoplasmic side of the inner nuclear membrane. Deficiencies in lamin B1 and lamin B2 impair neurodevelopment, but distinct functions for the two proteins in the development and homeostasis of the CNS have been elusive. Here we show that embryonic depletion of lamin B1 in retinal progenitors and postmitotic neurons affects nuclear integrity, leads to the collapse of the laminB2 meshwork, impairs neuronal survival, and markedly reduces the cellularity of adult retinas. In stark contrast, a deficiency of lamin B2 in the embryonic retina has no obvious effect on lamin B1 localization or nuclear integrity in embryonic retinas, suggesting that lamin B1, but not lamin B2, is strictly required for nucleokinesis during embryonic neurogenesis. However, the absence of lamin B2 prevents proper lamination of adult retinal neurons, impairs synaptogenesis, and reduces cone photoreceptor survival. We also show that lamin B1 and lamin B2 are extremely long-lived proteins in rod and cone photoreceptors. OF interest, a complete absence of both proteins during postnatal life has little or no effect on the survival and function of cone photoreceptors.

Original languageEnglish
Pages (from-to)1928-1937
Number of pages10
JournalMolecular biology of the cell
Volume27
Issue number12
DOIs
StatePublished - Jun 15 2016

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