Krüger M, Fischer R
Philipps Universität Marburg, Laboratorium für Mikrobiologie and Max-Planck-Institut für terrestrische Mikrobiologie, Marburg, Germany.
Genetics. 1996 Oct;144(2):533-40. doi: 10.1093/genetics/144.2.533.
Aspergillus nidulans reproduces asexually with single nucleated conidia. In apsA (anucleate primary sterigmata) strains, nuclear positioning is affected and conidiation is greatly reduced. To get further insights into the cellular functions of apsA, aconidial apsA strains were mutagenized and conidiating suppressor strains were isolated. The suppressors fell into two complementation groups, samA and samB (suppressor of anucleate metulae), samA mapped on linkage group 1 close to pyrG. The mutant allele was dominant in diploids homozygous for apsA. Viability of conidia of samA suppressor strains (samA-; apsA-) was reduced to 50% in comparison to wild-type conidia. Eighty percent of viable spores produced small size colonies that were temperature and benomyl-sensitive. samB mapped to chromosome VIII and was recessive. Viability of conidia from samB suppressor strains (apsA-; samB) was also affected but no small size colonies were observed. Both suppressors produced partial defects in sexual reproduction and both suppressed an apsA deletion mutation. In wild-type background the mutant loci affected hyphal growth rate (samA) or changed the colony morphology (samB) and inhibited sexual spore formation (samA and samB). Only subtle effects on conidiation were found. We conclude that both suppressor genes bypass the apsA function and are involved in microtubule-dependent processes.
构巢曲霉通过单核分生孢子进行无性繁殖。在apsA(无核初级分生孢子梗)菌株中,核定位受到影响,分生孢子形成大大减少。为了进一步深入了解apsA的细胞功能,对无分生孢子的apsA菌株进行诱变,并分离出分生孢子形成的抑制菌株。这些抑制菌株分为两个互补组,即samA和samB(无核小梗的抑制子),samA定位于与pyrG相邻的第1连锁群上。突变等位基因在apsA纯合二倍体中呈显性。与野生型分生孢子相比,samA抑制菌株(samA-; apsA-)的分生孢子活力降低到50%。80%的有活力孢子产生了对温度和苯菌灵敏感的小菌落。samB定位于第八条染色体上,呈隐性。来自samB抑制菌株(apsA-; samB)的分生孢子活力也受到影响,但未观察到小菌落。两种抑制子在有性生殖中都产生了部分缺陷,并且都抑制了apsA缺失突变。在野生型背景下,突变位点影响菌丝生长速率(samA)或改变菌落形态(samB),并抑制有性孢子形成(samA和samB)。仅发现对分生孢子形成有细微影响。我们得出结论,两个抑制基因都绕过了apsA的功能,并参与了微管依赖性过程。