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Gαi同源物gna-1控制粗糙脉孢菌中的多种分化途径。

The G alpha i homologue gna-1 controls multiple differentiation pathways in Neurospora crassa.

作者信息

Ivey F D, Hodge P N, Turner G E, Borkovich K A

机构信息

Department of Microbiology and Molecular Genetics, University of Texas-Houston Medical School 77030, USA.

出版信息

Mol Biol Cell. 1996 Aug;7(8):1283-97. doi: 10.1091/mbc.7.8.1283.

Abstract

Heterotrimeric G proteins are components of principal signaling pathways in eukaryotes. In higher organisms, alpha subunits of G proteins have been divided into four families, Gi, Gs, Gq, and G12. We previously identified a G alpha i homologue gna-1 in the filamentous fungus Neurospora crassa. Now we report that deletion of gna-1 leads to multiple phenotypes during the vegetative and sexual cycles in N. crassa. On solid medium, delta gna-1 strains have a slower rate of hyphal apical extension than wild type, a rate that is more pronounced under hyperosmotic conditions or in the presence of a cellophane overlay. delta gna-1 mutants accumulate less mass than wild-type strains, and their mass accumulation is not affected in the same way by exposure to light. delta gna-1 strains are defective in macroconidiation, possessing aerial hyphae that are shorter, contain abnormal swellings, and differentiate adherent macroconidia. During the sexual cycle, delta gna-1 strains are fertile as males. However, the mutants are female-sterile, producing small, aberrant female reproductive structures. After fertilization, delta gna-1 female structures do not enlarge and develop normally, and no sexual spores are produced. Thus, mutation of gna-1 results in sex-specific loss of fertility.

摘要

异源三聚体G蛋白是真核生物主要信号通路的组成部分。在高等生物中,G蛋白的α亚基已被分为四个家族,即Gi、Gs、Gq和G12。我们之前在丝状真菌粗糙脉孢菌中鉴定出一种Gαi同源物gna-1。现在我们报道,gna-1的缺失会导致粗糙脉孢菌营养生长和有性生殖周期出现多种表型。在固体培养基上,gna-1缺失菌株的菌丝顶端延伸速度比野生型慢,在高渗条件下或有玻璃纸覆盖时,这种速度差异更为明显。gna-1突变体积累的物质比野生型菌株少,并且它们的物质积累不受光照影响。gna-1缺失菌株在产大分生孢子方面存在缺陷,其气生菌丝较短,含有异常肿胀,且分化出附着的大分生孢子。在有性生殖周期中,gna-1缺失菌株作为雄性是可育的。然而,这些突变体作为雌性是不育的,产生小的、异常的雌性生殖结构。受精后,gna-1缺失的雌性结构不会正常扩大和发育,也不会产生有性孢子。因此,gna-1的突变导致了特定性别的育性丧失。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c92f/275978/db4cf541574d/mbc00015-0139-a.jpg

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