LéJohn H B
Can J Biochem Cell Biol. 1983 May;61(5):262-73. doi: 10.1139/o83-037.
Vegetatively growing cells of the coenocytic freshwater mould Achlya developed asexual sporangia and sporulated within 6 h of postransfer to a nutrient-free (starvation) medium. Sporangial development was arrested by the addition of L-glutamine to starving cells. During starvation (minus glutamine), three polyphosphate substances accumulated intracellularly, ATP was rapidly depleted, and a protein of molecular weight 42 000 (presumed to be actin) was actively synthesized, whereas synthesis of the most abundant detergent-soluble protein of molecular weight 83 000 (p83) ceased. In the presence of glutamine, starving cells used up the polyphosphates faster than they were formed. ATP depletion was delayed, cell calcium (Ca) exited rapidly, and synthesis of actin diminished while p83 synthesis continued unabated. Several pyrimidine analogues, including 5-diazouracil (which inhibited pyridimide nucleotide biosynthesis), and inorganic phosphate prevented Ca exit from glutamine-supplemented starving cells. The pyrimidine analogues delayed but did not inhibit sporangial development; however, they did not overcome glutamine suppression of sporangial development. Vegetatively growing and starving cells displayed significantly different protein synthesis patterns (monitored by polyacrylamide gel electrophoresis) but, when glutamine was added, it changed the protein synthesis pattern of starving cells to a form typical of vegetatively growing cells. Glutamine withdrawal reversed the effect and the cells differentiated. Pyrimidine analogues and inorganic phosphate did not alter the protein synthesis patterns of starving cells in the presence and absence of glutamine. The conclusion is that glutamine inhibition of sporangial development may be linked to its ability to subvert starving cell metabolism by making it vegetative like.
多核淡水霉菌绵霉营养生长的细胞在转移到无营养（饥饿）培养基后的6小时内发育出无性孢子囊并形成孢子。向饥饿的细胞中添加L - 谷氨酰胺会阻止孢子囊的发育。在饥饿期间（无谷氨酰胺），三种多聚磷酸物质在细胞内积累，ATP迅速耗尽，一种分子量为42000的蛋白质（推测为肌动蛋白）被积极合成，而分子量为83000的最丰富的去污剂可溶性蛋白质（p83）的合成停止。在有谷氨酰胺存在的情况下，饥饿的细胞消耗多聚磷酸的速度比其形成速度更快。ATP消耗延迟，细胞钙（Ca）迅速外流，肌动蛋白合成减少，而p83合成持续不减。几种嘧啶类似物，包括5 - 重氮尿嘧啶（抑制嘧啶核苷酸生物合成）和无机磷酸盐可阻止钙从添加谷氨酰胺的饥饿细胞中外流。嘧啶类似物延迟但不抑制孢子囊的发育；然而，它们不能克服谷氨酰胺对孢子囊发育的抑制作用。营养生长和饥饿的细胞表现出明显不同的蛋白质合成模式（通过聚丙烯酰胺凝胶电泳监测），但是当添加谷氨酰胺时，它将饥饿细胞的蛋白质合成模式改变为营养生长细胞典型的形式。谷氨酰胺撤除逆转了这种效应，细胞发生分化。在有和没有谷氨酰胺存在的情况下，嘧啶类似物和无机磷酸盐都不会改变饥饿细胞的蛋白质合成模式。结论是谷氨酰胺对孢子囊发育的抑制可能与其通过使其类似营养生长状态来颠覆饥饿细胞代谢的能力有关。
