NDC1 loss disrupts nuclear pores and halts meiosis in mouse oocytes

Deleting the gene Ndc1 in mouse oocytes leaves the animals female-sterile, according to a new study published in Cell Communication and Signaling. The work, led by Yi-Ke Lu, Bing-Wang Zhao and colleagues under senior author Zhen-Bo Wang, shows that NDC1, a transmembrane nucleoporin previously implicated in nuclear pore complex assembly, is required for normal oocyte maturation and meiotic progression in mammals.

The researchers used Gdf9-Cre to delete Ndc1 specifically in mouse oocytes. The resulting conditional knockout females were sterile, and their oocytes showed delayed germinal vesicle breakdown, arrest at meiosis I, and severe spindle defects. These outcomes establish that NDC1 is essential for the nuclear events that drive an oocyte through the divisions of meiosis.

Examination of the nuclear envelope revealed the likely structural basis of these failures. Ndc1 conditional knockout oocytes showed a marked loss of ALADIN protein and nuclear envelope signal, reduced enrichment of the nucleoporin NUP160 at the nuclear envelope, and fewer morphologically identifiable nuclear pore complexes. Notably, abnormal localization of ALADIN and NUP160 was already evident in growing oocytes from postnatal day 14 mice, indicating that the defect arises early during oocyte growth rather than only during maturation.

Nuclear pore complexes mediate transport between the nucleus and cytoplasm, and the study found that this transport was impaired but not abolished. Nuclear accumulation of Cyclin B1 and of an SV40 NLS reporter was delayed in Ndc1 conditional knockout oocytes, although nuclear import was not completely blocked. Ndc1 deletion also altered the distribution of the RBD-mCherry RanGTP reporter and of endogenous importin β, pointing to disruption of the RanGTP gradient that helps organize nuclear and spindle events.

The spindle defects were accompanied by changes in key regulators of microtubule organization. During early spindle assembly, TPX2 fluorescence in the spindle region and phosphorylated PLK1 fluorescence at acentriolar microtubule organizing centers increased, whereas phosphorylated Aurora A fluorescence at these sites decreased. The authors propose that impaired nuclear import together with these changes in spindle regulators may contribute to the meiotic defects observed after Ndc1 loss.

As the authors summarize, NDC1 is required for normal nuclear pore complex organization and meiotic progression in mouse oocytes. The findings come from a mouse genetic model, and the study was published as an open-access research article on 28 October 2026, shared early as a peer-reviewed, citable version of record in progress.

Subject of Research: The role of the nucleoporin NDC1 in nuclear pore complex organization and meiotic progression in mouse oocytes

Article Title: NDC1 is required for nuclear pore complex organization and meiotic progression in mouse oocytes

Article References: Lu, Y.-K., Zhao, B.-W., Guo, J.-N., Sun, S.-M., Xu, Y.-H., Yang, X.-M., Jiang, C., Li, W.-L., & Wang, Z.-B. (2026). NDC1 is required for nuclear pore complex organization and meiotic progression in mouse oocytes. Cell Communication and Signaling. https://doi.org/10.1186/s12964-026-03316-x

Image Credits: AI Generated

DOI: 10.1186/s12964-026-03316-x

Keywords: NDC1, nuclear pore complex, mouse oocytes, meiosis, oocyte maturation, nuclear import, ALADIN, NUP160, spindle defects, female fertility, nucleoporin, RanGTP