The pot1+ homologue in Aspergillus nidulans is required for ordering mitotic events.

Orderly progression through mitosis is essential to reduce segregation errors in the cell's genetic material. We have used a cytological screen to identify a mutant that progresses through mitosis aberrantly and have cloned the complementing gene, nimU, which encodes a protein related to Pot1 and other telomere end-binding proteins. We show that loss of nimU function leads to premature mitotic spindle elongation, premature mitotic exit, errors in chromosome segregation, and failure to delay mitotic exit under conditions that normally evoke the mitotic spindle checkpoint response. Whereas premature mitotic exit is dependent upon anaphase promoting complex function, premature spindle elongation is not. We conclude that nimU is constitutively required for orderly mitotic progression under normal growth conditions and also required for the conditional mitotic spindle checkpoint response.