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影响构巢曲霉孢子形成和柄曲霉素生物合成的显性突变。

Dominant mutations affecting both sporulation and sterigmatocystin biosynthesis in Aspergillus nidulans.

作者信息

Wieser J, Yu J H, Adams T H

机构信息

Department of Biology, Texas A & M University, College Station 77843, USA.

出版信息

Curr Genet. 1997 Sep;32(3):218-24. doi: 10.1007/s002940050269.

DOI:10.1007/s002940050269
PMID:9339347
Abstract

The initiation of conidiophore development in the filamentous fungus Aspergillus nidulans is a complex process requiring the activities of several genes including fluG, flbA, flbB, flbC, flbD, and flbE. Recessive mutations in any one of these genes result in greatly reduced expression of the brlA developmental regulatory gene and a colony morphology described as fluffy. These fluffy mutants have somewhat diverse phenotypes but generally grow as undifferentiated masses of vegetative hyphae to form large cotton-like colonies. In this paper we describe a genetic screen to identify dominant mutations resulting in similar fluffy colony morphologies. We have identified 36 dominant fluffy mutant strains and shown that 29 of these mutants have greatly reduced brlA expression as compared to wild-type. In addition, we have found that 19 of these mutants are not only developmentally altered but also fail to produce the toxic, carcinogenic, secondary metabolite sterigmatocystin. At least three of the mutants isolated result from dominant activating mutations in fadA which encodes the G alpha subunit of a heterotrimeric G-protein. Another of the mutants results from a dominant interfering mutation in brlA. We discuss the approaches taken to characterize these potentially important regulators of growth, development and secondary metabolism.

摘要

丝状真菌构巢曲霉分生孢子梗发育的起始是一个复杂的过程,需要包括fluG、flbA、flbB、flbC、flbD和flbE在内的几个基因的参与。这些基因中任何一个的隐性突变都会导致brlA发育调控基因的表达大幅降低,并产生一种被描述为蓬松的菌落形态。这些蓬松突变体具有一些不同的表型,但通常以未分化的营养菌丝团生长,形成大型棉絮状菌落。在本文中,我们描述了一种遗传筛选方法,以鉴定导致类似蓬松菌落形态的显性突变。我们已经鉴定出36个显性蓬松突变体菌株,并表明其中29个突变体与野生型相比,brlA表达大幅降低。此外,我们发现其中19个突变体不仅在发育上发生了改变,而且无法产生有毒、致癌的次生代谢产物柄曲霉素。分离得到的突变体中至少有三个是由fadA中的显性激活突变导致的,fadA编码一种异源三聚体G蛋白的Gα亚基。另一个突变体是由brlA中的显性干扰突变导致的。我们讨论了用于表征这些潜在的生长、发育和次生代谢重要调节因子的方法。

相似文献

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Dominant mutations affecting both sporulation and sterigmatocystin biosynthesis in Aspergillus nidulans.影响构巢曲霉孢子形成和柄曲霉素生物合成的显性突变。
Curr Genet. 1997 Sep;32(3):218-24. doi: 10.1007/s002940050269.
2
Aspergillus sporulation and mycotoxin production both require inactivation of the FadA G alpha protein-dependent signaling pathway.曲霉的孢子形成和霉菌毒素产生均需要使依赖FadA Gα蛋白的信号通路失活。
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flbD encodes a Myb-like DNA-binding protein that coordinates initiation of Aspergillus nidulans conidiophore development.flbD编码一种类Myb DNA结合蛋白,该蛋白协调构巢曲霉分生孢子梗发育的起始。
Genes Dev. 1995 Feb 15;9(4):491-502. doi: 10.1101/gad.9.4.491.
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Mutations in sfdA and sfdB suppress multiple developmental mutations in Aspergillus nidulans.sfdA和sfdB中的突变可抑制构巢曲霉中的多种发育突变。
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Overexpression of flbA, an early regulator of Aspergillus asexual sporulation, leads to activation of brlA and premature initiation of development.flbA是构巢曲霉无性孢子形成的早期调节因子,其过表达会导致brlA激活和发育的过早启动。
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FluG and flbA function interdependently to initiate conidiophore development in Aspergillus nidulans through brlA beta activation.在构巢曲霉中,FluG和flbA通过激活brlAβ相互依赖地发挥作用,以启动分生孢子梗的发育。
EMBO J. 1996 Jan 15;15(2):299-309.
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Correlation between the regulation of sterigmatocystin biosynthesis and asexual and sexual sporulation in Emericella nidulans.构巢曲霉中柄曲霉素生物合成调控与无性和有性孢子形成之间的相关性。
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Extragenic suppressors of loss-of-function mutations in the aspergillus FlbA regulator of G-protein signaling domain protein.曲霉属真菌G蛋白信号结构域蛋白FlbA功能缺失突变的基因外抑制子
Genetics. 1999 Jan;151(1):97-105. doi: 10.1093/genetics/151.1.97.

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