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gprA和gprB基因编码构巢曲霉自交所需的假定G蛋白偶联受体。

The gprA and gprB genes encode putative G protein-coupled receptors required for self-fertilization in Aspergillus nidulans.

作者信息

Seo Jeong-Ah, Han Kap-Hoon, Yu Jae-Hyuk

机构信息

Department of Food Microbiology and Toxicology, Food Research Institute, University of Wisconsin, Madison, WI 53706, USA.

出版信息

Mol Microbiol. 2004 Sep;53(6):1611-23. doi: 10.1111/j.1365-2958.2004.04232.x.

Abstract

The filamentous fungus Aspergillus nidulans possesses both asexual and sexual reproductive cycles. Sexual fruiting bodies (cleistothecia) can be formed in both homothallic (self) and heterothallic (outcross) conditions. In this study, we characterized two genes, gprA and gprB, that are predicted to encode putative G protein-coupled receptors (GPCRs) similar to fungal pheromone receptors. Deletion (Delta) of gprA or gprB resulted in the production of a few small cleistothecia carrying a reduced number of ascospores, whereas DeltagprADeltagprB eliminated fruiting body formation in homothallic conditions. However, nullifying gprA and/or gprB did not affect vegetative growth, asexual sporulation, Hülle cell formation or even cleistothecia formation in outcross, indicating that GprA and GprB are specifically required for self-fertilization. The gprA and gprB genes encode two transcripts and, for both genes, larger transcripts are detectable during vegetative growth and asexual development whereas smaller transcripts accumulate during sexual development. Upregulation of nsdD encoding a key sexual developmental activator resulted in the production of barren cleistothecia in the DeltagprADeltagprB mutant, suggesting that NsdD can partially rescue the developmental defects caused by deletion of GPCRs and that GprA/B-mediated signalling may activate other genes necessary for maturation of cleistothecia and ascosporogenesis. Deletion of gprA and/or gprB suppressed growth defects caused by DeltagprD, implying that GprA/B function downstream of GprD-mediated negative control of sexual development.

摘要

丝状真菌构巢曲霉具有无性和有性生殖周期。有性子实体(闭囊壳)可在同宗配合(自体受精)和异宗配合(杂交)条件下形成。在本研究中,我们对两个基因gprA和gprB进行了表征,预测它们编码与真菌信息素受体相似的假定G蛋白偶联受体(GPCR)。缺失gprA或gprB会导致产生一些带有较少子囊孢子的小闭囊壳,而缺失gprA和gprB则会在同宗配合条件下消除子实体形成。然而,使gprA和/或gprB失活并不影响营养生长、无性孢子形成、壳细胞形成,甚至在杂交中闭囊壳的形成,这表明GprA和GprB是自体受精所特需的。gprA和gprB基因编码两种转录本,对于这两个基因,较大的转录本在营养生长和无性发育过程中可检测到,而较小的转录本在有性发育过程中积累。编码关键有性发育激活因子的nsdD的上调导致缺失gprA和gprB的突变体中产生不育闭囊壳,这表明NsdD可以部分挽救因缺失GPCR而导致的发育缺陷,并且GprA/B介导的信号传导可能激活闭囊壳成熟和子囊孢子形成所需的其他基因。缺失gprA和/或gprB抑制了由缺失gprD引起的生长缺陷,这意味着GprA/B在GprD介导的有性发育负调控的下游发挥作用。

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