Sara Carvalhal, Michelle Stevense, Katrin Koehler, Ronald Naumann, Angela Huebner, Rolf Jessberger, Eric Griffis
ALADIN is a nuclear pore complex protein and this lab have previously investigated its role in mitosis due to it popping up in an RNAi screen for errors in spindle assembly and morphology in S2 cells. The gene for ALADIN (AAAS) is mutated in triple A syndrome, an autosomal-recessive disease comprising ACTH-resistant adrenal insufficiency, achalasia and alacrima symptoms. Aaas knockout mice are viable, but the females are sterile. Previous work (Carvalhal et al., 2015; 10.1091/mbc.E15-02-0113), showed that ALADIN has a complex role in mitosis in somatic cells and the question arises: does it have a function in meiotic spindles in oocytes. This preprint delves into this question and shows that ALADIN is needed for spindle positioning as well as spindle assembly. In knockout oocytes polar body extrusion is impaired. Following oocytes after in-vitro fertilization shows that knockouts fail to progress, with only 1 out of 15 observed making it to the two-cell stage, but progressing no further. These results are more striking than the mitotic problems observed in somatic cells after RNAi. A possible explanation is the size of the spindles relative to the size of the cell. Recently, a concept has emerged where, in cells with open mitosis, the components to build a mitotic spindle are concentrated by a ‘nuclear envelope-like’ structure (Schweitzer et al., 2015; 10.1083/jcb.201506107). The images in Carvalhal show ALADIN wrapping around the spindle in oocytes and suggest that it may have a role in maintaining this exclusion zone.
-Stephen J. Royle, University of Warwick