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MOD-D是粪生粪壳菌的一种Gα亚基,参与发育调控和营养体不亲和性。

MOD-D, a Galpha subunit of the fungus Podospora anserina, is involved in both regulation of development and vegetative incompatibility.

作者信息

Loubradou G, Bégueret J, Turcq B

机构信息

Laboratoire de Génétique Moléculaire des Champignons Filamenteux, Institut de Biochimie et de Génétique Cellulaires, CNRS UPR 9026, 33077 Bordeaux, France.

出版信息

Genetics. 1999 Jun;152(2):519-28. doi: 10.1093/genetics/152.2.519.

Abstract

Cell death via vegetative incompatibility is widespread in fungi but molecular mechanism and biological function of the process are poorly understood. One way to investigate this phenomenon was to study genes named mod that modified incompatibility reaction. In this study, we cloned the mod-D gene that encodes a Galpha protein. The mod-D mutant strains present developmental defects. Previously, we showed that the mod-E gene encodes an HSP90. The mod-E1 mutation suppresses both vegetative incompatibility and developmental defects due to the mod-D mutation. Moreover, we isolated the PaAC gene, which encodes an adenylate cyclase, as a partial suppressor of the mod-D1 mutation. Our previous results showed that the molecular mechanisms involved in vegetative incompatibility and developmental pathways are connected, suggesting that vegetative incompatibility may result from disorders in some developmental steps. Our new result corroborates the involvement of mod genes in signal transduction pathways. As expected, we showed that an increase in the cAMP level is able to suppress the defects in vegetative growth due to the mod-D1 mutation. However, cAMP increase has no influence on the suppressor effect of the mod-D1 mutation on vegetative incompatibility, suggesting that this suppressor effect is independent of the cAMP pathway.

摘要

通过营养体不亲和性导致的细胞死亡在真菌中广泛存在,但该过程的分子机制和生物学功能却知之甚少。研究这一现象的一种方法是研究名为mod的修饰不亲和反应的基因。在本研究中,我们克隆了编码Gα蛋白的mod-D基因。mod-D突变体菌株存在发育缺陷。此前,我们表明mod-E基因编码一种HSP90。mod-E1突变可抑制由于mod-D突变导致的营养体不亲和性和发育缺陷。此外,我们分离出了编码腺苷酸环化酶的PaAC基因,作为mod-D1突变的部分抑制因子。我们之前的结果表明,营养体不亲和性和发育途径所涉及的分子机制是相互关联的,这表明营养体不亲和性可能是由某些发育步骤的紊乱导致的。我们的新结果证实了mod基因参与信号转导途径。正如预期的那样,我们表明cAMP水平的升高能够抑制由于mod-D1突变导致的营养生长缺陷。然而,cAMP升高对mod-D1突变对营养体不亲和性的抑制作用没有影响,这表明这种抑制作用独立于cAMP途径。

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