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Regulation of L-phenylalanine ammonia-lyase by L-phenylalanine and nitrogen in Neurospora crassa.

机译:L.-苯丙氨酸和氮在神经孢菌中对L-苯丙氨酸氨裂解酶的调节。

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摘要

Neurospora crassa possesses an inducible L-phenylalanine ammonia-lyase that is expressed only when cells are derepressed for nitrogen in the presence of L-phenylalanine. Enzyme synthesis requires both induction by L-phenylalanine and simultaneous nitrogen catabolite derepression. Carbon limitation in the presence of phenylalanine does not elicit induction of L-phenylalanine ammonia-lyase. Specific induction by L-phenylalanine is required, and other amino acids completely failed to induce any lyase activity. The nit-2 gene is a major regulatory locus which is believed to mediate nitrogen catabolite repression in Neurospora. Mutants of nit-2 fail to express any phenylalanine ammonia-lyase activity under conditions of derepression and induction which lead to good enzyme induction in the wild type and in nit-2 revertants. The loss of lyase activity in nit-2 mutants does not result from inducer exclusion, which suggests that the nit-2 gene product has a direct role in controlling the expression of this enzyme. Substantial amounts of the enzyme were detected in the growth medium as well as in cell extracts. Inhibitors of protein synthesis or RNA synthesis block the induction of L-phenylalanine ammonia-lyase, suggesting that expression of this enzyme is controlled at the level of transcription.
机译:景天孢子虫具有可诱导的L-苯丙氨酸氨裂合酶,仅当在L-苯丙氨酸存在的情况下细胞对氮的阻遏作用时才会表达。酶的合成既需要L-苯丙氨酸的诱导,又需要氮分解代谢物的阻抑作用。苯丙氨酸存在下的碳限制不会引起L-苯丙氨酸氨解酶的诱导。需要通过L-苯丙氨酸进行特异性诱导,而其他氨基酸完全不能诱导任何裂解酶活性。 nit-2基因是一个主要的调控基因座,据信可介导Neurospora中的氮分解代谢物阻遏。 nit-2突变体在抑制和诱导条件下无法表达任何苯丙氨酸氨解酶活性,这在野生型和nit-2回复株中导致良好的酶诱导。 nit-2突变体中裂解酶活性的丧失不是由诱导物排斥引起的,这表明nit-2基因产物在控制该酶的表达中具有直接作用。在生长培养基以及细胞提取物中检测到大量的酶。蛋白质合成或RNA合成的抑制剂会阻止L-苯丙氨酸氨解酶的诱导,这表明该酶的表达受转录水平的控制。

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