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构巢曲霉中areA基因在氮代谢调控中的作用研究。

Studies on the role of the areA gene in the regulation of nitrogen catabolism in Aspergillus nidulans.

作者信息

Hynes M J

出版信息

Aust J Biol Sci. 1975 Jun;28(3):301-13. doi: 10.1071/bi9750301.

Abstract

Mutants of Apergillus nidulans with lesions in a gene, areA (formerly called amdT), have been isolated by a variety of different selection methods. The areA mutants show a range of pleiotropic growth responses to a number of compounds as sole nitrogen sources, but are normal in utilization of carbon sources. The levels of two amidase enzymes as well as urease have been investigated in the mutants and have been shown to be affected by this gene. Most of the areA mutants have much lower amidase-specific activities when grown in ammonium-containing medium, compared with mycelium incubated in medium lacking a nitrogen source. Some of the areA mutants do not show derepression of urease upon relief of ammonium repression. The dominance relationships of areA alleles have been investigated in heterozygous diploids, and these studies lend support to the proposal that areA codes for a positively acting regulatory product. One of the new areA alleles is partially dominant to areA+ and areA102. This may be a result of negative complementation or indicate that areA has an additional negative regulatory function. Investigation of various amdR; areA double mutants has led to the conclusion that amdR and areA participate in independent regulatory circuits in the control of acetamide utilization. Studies on an amdRc; areA double mutant indicate that areA is involved in derepression of acetamidase upon relief of ammonium repression.

摘要

通过多种不同的选择方法,已分离出构巢曲霉中一个名为areA(以前称为amdT)的基因发生损伤的突变体。areA突变体对多种作为唯一氮源的化合物表现出一系列多效性生长反应,但在碳源利用方面是正常的。已对突变体中的两种酰胺酶以及脲酶的水平进行了研究,结果表明它们受该基因影响。与在缺乏氮源的培养基中培养的菌丝体相比,大多数areA突变体在含铵培养基中生长时具有低得多的酰胺酶比活性。一些areA突变体在铵抑制解除后未表现出脲酶的去阻遏作用。已在杂合二倍体中研究了areA等位基因的显性关系,这些研究支持了areA编码一种正向作用调节产物的提议。其中一个新的areA等位基因对areA+和areA102具有部分显性。这可能是负互补的结果,或者表明areA具有额外的负调节功能。对各种amdR;areA双突变体的研究得出结论,amdR和areA在乙酰胺利用的控制中参与独立的调节途径。对amdRc;areA双突变体的研究表明,areA在铵抑制解除后参与乙酰胺酶的去阻遏作用。

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