Regulation of progenitor cell survival by a novel chromatin remodeling factor during neural tube development

During development, progenitor cell survival is essential for proper tissue functions, but the underlying mechanisms are not fully understood. Here we show that ERCC6L2, a member of the Snf2 family of helicase‐like proteins, plays an essential role in the survival of developing chick neural cells. E...

Full description

Saved in:
Bibliographic Details
Published inDevelopment, growth & differentiation Vol. 66; no. 1; pp. 89 - 100
Main Authors Sasai, Noriaki, Tada, Shogo, Ohshiro, Jumi, Kogiso, Chikara, Shinozuka, Takuma
Format Journal Article
LanguageEnglish
Published Japan Wiley Subscription Services, Inc 01.01.2024
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:During development, progenitor cell survival is essential for proper tissue functions, but the underlying mechanisms are not fully understood. Here we show that ERCC6L2, a member of the Snf2 family of helicase‐like proteins, plays an essential role in the survival of developing chick neural cells. ERCC6L2 expression is induced by the Sonic Hedgehog (Shh) signaling molecule by a mechanism similar to that of the known Shh target genes Ptch1 and Gli1. ERCC6L2 blocks programmed cell death induced by Shh inhibition and this inhibition is independent of neural tube patterning. ERCC6L2 knockdown by siRNA resulted in the aberrant appearance of apoptotic cells. Furthermore, ERCC6L2 cooperates with the Shh signal and plays an essential role in the induction of the anti‐apoptotic factor Bcl‐2. Taken together, ERCC6L2 acts as a key factor in ensuring the survival of neural progenitor cells. During neural tube development, the balance between cell selection and survival is important to determine the size of the organ. In this report, we describe a novel helicase‐like protein, ERCC6L2, whose expression is induced by the Sonic Hedgehog signal, which promotes cell survival.
Bibliography:Shogo Tada, Jumi Ohshiro, and Chikara Kogiso contributed equally to this work.
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0012-1592
1440-169X
DOI:10.1111/dgd.12905