Arst H N, MacDonald D W
Mol Gen Genet. 1978 Jul 6;163(1):17-22. doi: 10.1007/BF00268959.
The prn gene cluster involved in L-proline catabolism in Aspergillus nidulans, has the gene order prnA-prnD-regulatory region-prnB-prnC. prnB, prnD, and prnC specify proline permease, proline oxidase, and delta1-pyrroline-5-carboxylate (P5C) dehydrogenase, respectively. prnA is probably a positive regulatory gene whose product is necessary for expression of the prn activities. Proline induces proline permease and P5C dehydrogenase in prnD- mutants which lack proline oxidase, showing that proline does not have to be converted to P5C to act as inducer. Deletion mutations extending from within prnD to within prnB result in considerably reduced expression of prnC, whereas a prnD- prnB- double mutant shows normal prnC expression. This strongly suggests that the deletion mutations eliminate a promotor/initiator site for transcription of a dicistronic messenger for prnB and prnC. The fact that the deletions do not eliminate prnC expression altogether indicates that at least one other species of prnC transcript (monocistronic, tricistronic, or tetracistronic) can be made.
构巢曲霉中参与L-脯氨酸分解代谢的prn基因簇,其基因顺序为prnA-prnD-调控区-prnB-prnC。prnB、prnD和prnC分别编码脯氨酸通透酶、脯氨酸氧化酶和Δ1-吡咯啉-5-羧酸(P5C)脱氢酶。prnA可能是一个正向调控基因,其产物是prn活性表达所必需的。脯氨酸可诱导缺乏脯氨酸氧化酶的prnD-突变体中的脯氨酸通透酶和P5C脱氢酶,这表明脯氨酸不必转化为P5C即可作为诱导剂。从prnD内部延伸至prnB内部的缺失突变会导致prnC的表达大幅降低,而prnD- prnB-双突变体则显示出正常的prnC表达。这强烈表明缺失突变消除了prnB和prnC双顺反子信使转录的启动子/起始位点。缺失突变并未完全消除prnC表达这一事实表明,至少可以产生另一种prnC转录本(单顺反子、三顺反子或四顺反子)。