Harris S D, Hamer L, Sharpless K E, Hamer J E
Department of Microbiology, University of Connecticut Health Center, Farmington 06030-3205, USA.
EMBO J. 1997 Jun 16;16(12):3474-83. doi: 10.1093/emboj/16.12.3474.
Cytokinesis (septation) in the fungus Aspergillus nidulans occurs through the formation of a transient actin ring at the incipient division site. Temperature-sensitive mutations in the sepA gene prevent septation and cause defects in the maintenance of cellular polarity, without affecting growth and nuclear division. The sepA gene encodes a member of the growing family of FH1/2 proteins, which appear to have roles in morphogenesis and cytokinesis in organisms such as yeast and Drosophila. Results from temperature shift and immunofluorescence microscopy experiments strongly suggest that sepA function requires a preceding mitosis and that sepA acts prior to actin ring formation. Deletion mutants of sepA exhibit temperature-sensitive growth and severe delays in septation at the permissive temperature, indicating that expression of another gene may compensate for the loss of sepA. Conidiophores formed by sepA mutants exhibit abnormal branching of the stalk and vesicle. These results suggest that sepA interacts with the actin cytoskeleton to promote formation of the actin ring during cytokinesis and that sepA is also required for maintenance of cellular polarity during hyphal growth and asexual morphogenesis.
构巢曲霉中的胞质分裂（隔膜形成）通过在初始分裂位点形成一个短暂的肌动蛋白环来进行。sepA基因中的温度敏感突变会阻止隔膜形成，并导致细胞极性维持方面的缺陷，但不影响生长和核分裂。sepA基因编码FH1/2蛋白不断增加的家族中的一个成员，这类蛋白似乎在酵母和果蝇等生物体的形态发生和胞质分裂中发挥作用。温度转换和免疫荧光显微镜实验的结果强烈表明，sepA功能需要先有一次有丝分裂，并且sepA在肌动蛋白环形成之前起作用。sepA的缺失突变体在允许温度下表现出温度敏感型生长和隔膜形成的严重延迟，这表明另一个基因的表达可能补偿了sepA的缺失。sepA突变体形成的分生孢子梗表现出梗和囊泡的异常分支。这些结果表明，sepA在胞质分裂过程中与肌动蛋白细胞骨架相互作用以促进肌动蛋白环的形成，并且在菌丝生长和无性形态发生过程中维持细胞极性也需要sepA。
