Sanchez J, Hardisson C
Can J Microbiol. 1979 Jul;25(7):833-40. doi: 10.1139/m79-123.
Synthesis of beta-galactosidase by Streptomyces violaceus was induced by D-galactose and L-arabinose, and to a lesser extent by lactose, D-arabinose, and methyl-beta-D-galactopyranoside. The synthesis of the enzyme was linear and started to increase 2--3 h after induction by galactose, reaching a maximum after 5--7 h. The highest level of specific activity was observed in 2% galactose, with an increase of 45 times over the basal level in glycerol. Isopropyl-beta-D-thiogalactopyranoside (IPTG) and methyl-beta-D-thiogalactopyranoside (TMG) inhibited induction by D-galactose, but did not influence enzymatic activity. Cellular extracts hydrolyzed O-nitrophenyl-beta-D-galactopyranoside, but did not significantly hydrolyze lactose, melibiose, p-nitrophenyl-alpha-D-galactopyranoside, p-nitrophenyl-beta-D-fucoside, or p-nitrophenyl-beta-D-glucopyranoside. Rifampicin and chloramphenicol inhibited beta-galactosidase synthesis in non-preinduced and in preinduced cells. The inhibition by chloramphenicol was reversible.
紫色链霉菌合成β-半乳糖苷酶是由D-半乳糖和L-阿拉伯糖诱导的，乳糖、D-阿拉伯糖和甲基-β-D-吡喃半乳糖苷的诱导作用较弱。该酶的合成呈线性，在半乳糖诱导后2-3小时开始增加，5-7小时后达到最大值。在2%的半乳糖中观察到最高水平的比活性，比在甘油中的基础水平增加了45倍。异丙基-β-D-硫代半乳糖苷（IPTG）和甲基-β-D-硫代半乳糖苷（TMG）抑制D-半乳糖的诱导，但不影响酶活性。细胞提取物能水解O-硝基苯基-β-D-吡喃半乳糖苷，但对乳糖、蜜二糖、对硝基苯基-α-D-吡喃半乳糖苷、对硝基苯基-β-D-岩藻糖苷或对硝基苯基-β-D-吡喃葡萄糖苷的水解作用不明显。利福平和平氯霉素抑制未预诱导和预诱导细胞中β-半乳糖苷酶的合成。氯霉素的抑制作用是可逆的。
