Abstract
During spermiogenesis, haploid round spermatids differentiate into spermatozoa. This involves nuclear elongation, chromatin compaction, cytoplasm reduction, and formation of the acrosome and the flagellum. These events are orchestrated by cytoskeletal elements - acroplaxome and manchette - that attach to the nuclear envelope (NE) except at the caudal pole where the nuclear pore complexes (NPCs) shift to form a dense array. Here, we use a genetic dissection approach to reveal function at the caudal NE, through the study of two spermatid-specific proteins, whose human orthologues persist there as spermatids elongate: NUP210L, a transmembrane nucleoporin and BAF-L, paralogue and interactor of chromatin protein BAF. In mice, inactivation of either BAF-L or NUP210L has no impact on fertility. However, we show here that in mice lacking NUP210L, two copies of BAF-L become essential for fertility; in Nup210l−/−,Banf2+/− or Nup210l−/−,Banf2−/− mice, most spermatids arrest during nuclear elongation (step 10-11) with mislocalized NPCs and disorganized manchette microtubules that frequently invaginate the nucleus from the caudal pole. Our results suggest that the NPC array, and BAF-L/BAF, ensure nuclear integrity at the caudal pole during spermatid remodeling.
Summary: Nucleoporin NUP210L and BAF-paralogue BAF-L function redundantly during mouse spermatid nuclear remodeling to concentrate nuclear pores to the flagellar pole, organize the manchette cytoskeleton and prevent nuclear invagination by microtubules.
Competing Interest Statement
The authors have declared no competing interest.
Footnotes
This version has only received minor revision to correct errors in formatting of references and citations. The title and Abstract have been modified to make them shorter. Keywords have been changed. A brief Summary Statement has been added. We have uploaded all supplementary files referred to in the manuscript. These were not available in the previous version.
