Targeted inactivation of nuclear interaction partner of ALK disrupts meiotic prophase

• DOI: 10.1242/dev.073072
• Publication Date: 2012-06-14T01:39:01Z
• Authors: Anna Lena Illert; Hiroyuki Kawaguchi; Cristina Antinozzi; Florian Bassermann; Letitia Quintanil...; Christine von Kli...; Mitsuteru Hiwatari; Christian Peschel; Dirk G. de Rooij; Stephan W. Morris; Marco Barchi; Justus Duyster
• Keywords: Synapsis; Cyclin B1

NIPA (nuclear interaction partner of ALK) is an F-box-like protein that monitors the timing mitotic entry. Constitutively active delays entry by preventing accumulation nuclear cyclin B1. Here, we have investigated consequences Nipa inactivation using a conditional knockout strategy. Nipa-deficient animals are viable but show lower birth rate and reduced body weight. Furthermore, males sterile owing to block spermatogenesis during meiotic prophase. Whereas Nipa−/− mouse embryonic fibroblasts no severe phenotype, spermatocytes arrest stage IV epithelial cycle with subsequent TUNEL-positive apoptosis resulting from improper synapsis, defects in repair DNA double-stranded breaks synaptonemal complex formation. Moreover, B1 premature increase G2/M kinase activity spermatocytes. Together, these results reveal novel role for meiosis.