Zonneveld B J
Arch Microbiol. 1975 Oct 27;105(2):105-8. doi: 10.1007/BF00447122.
Aspergillus nidulans was completely devoid of fruit bodies when grown on manganese deficient cultures. This result was shown earlier to be due to a lack of alpha-1,3 glucan in the cell wall. Several enzymes of carbon and nitrogen metabolism were investigated in an attempt to explain the absence of this reserve material. Synthesis of glucose-6-phosphate dehydrogenase, phosphoglucoisomerase and aldolase, were not strongly affected by manganese deficiency. However, phosphoglucomutase showed only 60% of the activity of the control cultures and it was argued that this was connected with the low amounts of alpha-1,3 glucan synthesized. Malate dehydrogenase was the enzyme the least affected by manganese deficiency and the two to threefold higher activity measured after glucose depletion might indicate the induction of the glyoxylate cycle. An impaired glutamine synthetase could explain the increase in activity observed for NAD-glutamine dehydrogenase.
构巢曲霉在缺锰培养基上生长时完全没有子实体。先前的研究表明,这一结果是由于细胞壁中缺乏α-1,3-葡聚糖。为了解释这种储备物质的缺失,对几种碳氮代谢酶进行了研究。葡萄糖-6-磷酸脱氢酶、磷酸葡萄糖异构酶和醛缩酶的合成不受锰缺乏的强烈影响。然而,磷酸葡萄糖变位酶的活性仅为对照培养物的60%,有人认为这与合成的α-1,3-葡聚糖量低有关。苹果酸脱氢酶是受锰缺乏影响最小的酶,葡萄糖耗尽后测得的活性高出两到三倍,这可能表明乙醛酸循环被诱导。谷氨酰胺合成酶受损可以解释所观察到的NAD-谷氨酰胺脱氢酶活性增加的现象。