Paszewski A, Grabski J
J Bacteriol. 1975 Nov;124(2):893-904. doi: 10.1128/jb.124.2.893-904.1975.
In Aspergillus nidulans the pathway involving cystathionine formation is the main one for homocysteine synthesis. Mutants lacking cystathionine gamma-synthase or beta-cystathionase are auxotrophs suppressible by: (i) mutations in the main pathway of cysteine synthesis (cysA1, cysB1, and cysC1), (ii) mutations causing stimulation of cysteine catabolism (su101), and (iii) mutations in a presumed regulatory gene (suAmeth). A relative shortage of cysteine in the first group of suppressors causes a derepression of homocysteine synthase, the enzyme involved in the alternative pathway of homocysteine synthesis. A similar derepression is observed in the suAmeth strain. Homocysteine synthesized by this pathway serves as precursor for cysteine and methionine synthesis. A mutant with altered homocysteine synthase is a prototroph, indicating that this enzyme is not essential for the fungus.
在构巢曲霉中，涉及胱硫醚形成的途径是同型半胱氨酸合成的主要途径。缺乏胱硫醚γ-合酶或β-胱硫醚酶的突变体是营养缺陷型，可被以下因素抑制：（i）半胱氨酸合成主要途径中的突变（cysA1、cysB1和cysC1），（ii）导致半胱氨酸分解代谢受刺激的突变（su101），以及（iii）一个假定调控基因中的突变（suAmeth）。第一组抑制子中半胱氨酸的相对短缺导致同型半胱氨酸合酶（参与同型半胱氨酸合成替代途径的酶）的去阻遏。在suAmeth菌株中也观察到类似的去阻遏。通过该途径合成的同型半胱氨酸作为半胱氨酸和甲硫氨酸合成的前体。同型半胱氨酸合酶发生改变的突变体是原养型，这表明该酶对真菌并非必不可少。
