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本文引用的文献

1
Correlation between base-pair transition and complementation pattern in nitrous acid-induced ad-3B mutants of Neurospora crassa.
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2
Mutants affecting thymidine metabolism in Neurospora crassa.影响粗糙脉孢菌中胸苷代谢的突变体。
J Bacteriol. 1969 Oct;100(1):383-9. doi: 10.1128/jb.100.1.383-389.1969.
3
Negative cooperativity in regulatory enzymes.调节酶中的负协同性。
Proc Natl Acad Sci U S A. 1969 Apr;62(4):1121-8. doi: 10.1073/pnas.62.4.1121.
4
Ammonia inhibition of the general amino acid permease and its suppression in NADPH-specific glutamate dehydrogenaseless mutants of saccharomyces cerevisiae.氨对普通氨基酸通透酶的抑制作用及其在酿酒酵母NADPH特异性谷氨酸脱氢酶缺失突变体中的抑制解除。
Biochem Biophys Res Commun. 1972 Aug 21;48(4):749-56. doi: 10.1016/0006-291x(72)90670-5.
5
Isolation and characterization of a mutant of Neurospora crassa deficient in general amino acid permease activity.粗糙脉孢菌中一般氨基酸通透酶活性缺陷型突变体的分离与鉴定。
Biochim Biophys Acta. 1975 Nov 17;413(1):45-51. doi: 10.1016/0005-2736(75)90057-7.
6
Regulation of the purine catabolic enzymes in Neurospora crassa.粗糙脉孢菌中嘌呤分解代谢酶的调控
Arch Biochem Biophys. 1975 Feb;166(2):565-74. doi: 10.1016/0003-9861(75)90421-x.

粗糙脉孢菌中铵对尿嘧啶摄取的抑制作用。

Depression of uracil uptake by ammonium in Neurospora crassa.

作者信息

Magill J M, Edwards E S, Sabina R L, Magill C W

出版信息

J Bacteriol. 1976 Sep;127(3):1265-9. doi: 10.1128/jb.127.3.1265-1269.1976.

DOI:10.1128/jb.127.3.1265-1269.1976
PMID:134026
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC232919/
Abstract

The mechanism of uracil uptake and one aspect of its regulation were studied in germinated conidia of Neurospora crassa. Uracil was found to be taken up by a transport mechanism that did not exhibit Michaelis-Menten kinetics. Rather, the kinetic patterns indicated two separate systems or a single transport mechanism with negative cooperativity. Cytosine and thymine inhibited uracil uptake, but uridine did not. The mutant strain uc-5-pyr-1, which failed to transport uracil, was used in reversion studies and to map the uc-5 locus. Spontaneous reversion rates at the uc-5 locus were found to be approximately 2 x 10(-8), indicating that the uc-5 lesion results from a single mutation. Loss of the uracil transport function through a single mutation favors the model of a single transport mechanism with negative cooperativity. Uracil uptake was significantly decreased in the presence of NH 4+, and evidence is presented for repression by NH4+ of a uracil transport system. Growth rates of pyrimidine-requiring and wild-type strains measured in the presence and absence of NH4+, with uracil as the pyrimidine supplement, showed that NH4+ decreased the growth rates of the pyrimidine-requiring strains significantly, while having no effect on wild-type growth rates.

摘要

在粗糙脉孢菌的萌发分生孢子中研究了尿嘧啶摄取机制及其调控的一个方面。发现尿嘧啶通过一种不表现米氏动力学的转运机制被摄取。相反,动力学模式表明存在两个独立的系统或具有负协同性的单一转运机制。胞嘧啶和胸腺嘧啶抑制尿嘧啶摄取,但尿苷则不然。未能转运尿嘧啶的突变菌株uc - 5 - pyr - 1被用于回复突变研究和定位uc - 5位点。发现uc - 5位点的自发回复率约为2×10(-8),表明uc - 5损伤是由单个突变引起的。通过单个突变丧失尿嘧啶转运功能支持具有负协同性的单一转运机制模型。在存在NH4+的情况下,尿嘧啶摄取显著降低,并且有证据表明NH4+对尿嘧啶转运系统具有抑制作用。在有和没有NH4+的情况下,以尿嘧啶作为嘧啶补充物测量需要嘧啶的菌株和野生型菌株的生长速率,结果表明NH4+显著降低了需要嘧啶的菌株的生长速率,而对野生型生长速率没有影响。