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大肠杆菌的磷酸果糖激酶B(PfkB)和磷酸果糖激酶C(pfkC)基因座

PfkB and pfkC loci of Escherichia coli.

作者信息

Vinopal R T, Fraenkel D G

出版信息

J Bacteriol. 1975 Jun;122(3):1153-61. doi: 10.1128/jb.122.3.1153-1161.1975.

Abstract

Mutants lacking Escherichia coli phosphofructokinase (pfkA, 78 min) are suppressed by the unlinked pfkB1 mutation, which restores some enzyme activity (Morrissey and Fraenkel, 1972). We here describe a secondary mutation at pfkB, "PFKB-," which abolishes the suppression as well as the low residual activity of unsuppressed pfkA mutants. pfkB is at about 33 min. with the gene order groD-pps-pheS-pfkB. A positive selection was found that yielded both the pfkB-mutations and a new similar mutation, pfkC-. pfkC is an early marker in Hfr HL16(ca. 50 to 55 min). Some pfkC-, but no pfkB-, mutations were amber. A temperature-sensitive pfkB- was also obtained. Strains carrying pfkB- or pfkC-, but wild type at pfkA, were not markedly affected in growth on sugars. A new search for suppressors such as pfkB1 gave five independent candidates, all of which suppressed both pfkA1 and pfkA2 and occurred in the pfkB region; none occurred at pfkC. Neither the pfkB nor the pfkC loci have assigned functions. It is likely that they are somehow involved in expression of phosphofructokinase activity 2 (Fraenkel, Kotlarz, and Buc, 1973).

摘要

缺乏大肠杆菌磷酸果糖激酶(pfkA,78分钟处)的突变体可被不连锁的pfkB1突变所抑制,该突变可恢复一些酶活性(莫里西和弗伦克尔,1972年)。我们在此描述了pfkB处的一个二次突变,“PFKB-”,它消除了抑制作用以及未被抑制的pfkA突变体的低残留活性。pfkB位于约33分钟处,基因顺序为groD-pps-pheS-pfkB。发现了一种阳性选择,它能产生pfkB突变和一个新的类似突变,pfkC-。pfkC是Hfr HL16中的一个早期标记(约50至55分钟)。一些pfkC-突变,但没有pfkB-突变,是琥珀突变。还获得了一个温度敏感型的pfkB-。携带pfkB-或pfkC-但pfkA为野生型的菌株在糖上生长时没有受到明显影响。对诸如pfkB1这样的抑制子进行的新搜索得到了五个独立的候选者,它们都能抑制pfkA1和pfkA2,且都发生在pfkB区域;在pfkC处没有出现。pfkB和pfkC位点都没有确定的功能。它们可能以某种方式参与磷酸果糖激酶活性2的表达(弗伦克尔、科特拉兹和布克,1973年)。

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