Pendyala L, Wellman A M
Biochim Biophys Acta. 1980 Apr 30;607(2):350-60. doi: 10.1016/0005-2787(80)90087-8.
Purine biosynthesis and its regulation was studied in Neurospora crassa by the incorporation of label from [14C]formate into total cellular purines. In general, the purine biosynthesis resulted in slightly more cellular guanine than adenine nucleotides. The acid-soluble pool however, contained more adenine compounds than guanine. Exogenous adenine was found to be an effective regulatory of the proximal steps of the de novo biosynthesis, while both adenine and guanine were equally effective in regulating the branch point activities. 6-Methyl purine inhibited the proximal steps of the purine synthesis more effectively than the branch point leading to adenine biosynthesis. A 6-methyl purine resistant mutant, Mepr-10, with defective adenine phosphoribosyl pyrophosphate transferase showed no inhibition of purine synthesis by 6-methyl purine, while 6-methyl purine resistant strains Mepr-3 and Mepr-1 showed partial inhibition. It has been suggested that Mepr-3 and Mepr-1 may be mutants of glutamine amidotransferase with altered affinities for 6-methyl purine. The rate of purine biosynthesis increased during the first 8 h of incubation of conidia in minimal medium, after which it declined even though the growth continued.
通过将[14C]甲酸中的标记掺入总细胞嘌呤中，研究了粗糙脉孢菌中的嘌呤生物合成及其调控。一般来说，嘌呤生物合成产生的细胞鸟嘌呤比腺嘌呤核苷酸略多。然而，酸溶性池中的腺嘌呤化合物比鸟嘌呤更多。发现外源性腺嘌呤是从头生物合成近端步骤的有效调节剂，而腺嘌呤和鸟嘌呤在调节分支点活性方面同样有效。6-甲基嘌呤比导致腺嘌呤生物合成的分支点更有效地抑制嘌呤合成的近端步骤。一种具有缺陷的腺嘌呤磷酸核糖焦磷酸转移酶的6-甲基嘌呤抗性突变体Mepr-10对6-甲基嘌呤不显示嘌呤合成抑制，而6-甲基嘌呤抗性菌株Mepr-3和Mepr-1显示部分抑制。有人提出Mepr-3和Mepr-1可能是谷氨酰胺酰胺转移酶的突变体，对6-甲基嘌呤的亲和力发生了改变。在基本培养基中分生孢子培养的前8小时内，嘌呤生物合成速率增加，此后即使生长继续，其速率也下降。
