Rashid M H, Sekiguchi J
Department of Applied Biology, Faculty of Textile Science and Technology, Shinshu University, Nagano, Japan.
J Bacteriol. 1996 Nov;178(22):6640-3. doi: 10.1128/jb.178.22.6640-6643.1996.
A flaD (sinR) null mutation depressed sigD-lacZ expression only two- to fourfold, whereas a flaD1 point mutation depressed it almost completely. Introduction of pHYSigD, a sigmaD-overproducing plasmid, corrected the filamentous phenotype common to both sinR mutants; autolysin synthesis was restored partially and completely in the flaD1 and flaD (sinR) null strains, respectively. Flagellin synthesis and motility were not restored at all in either strain.
flaD（sinR）基因敲除突变使sigD - lacZ表达仅降低2至4倍，而flaD1点突变几乎完全抑制了其表达。引入sigmaD过量表达质粒pHYSigD可纠正两种sinR突变体共有的丝状表型；自溶素合成在flaD1和flaD（sinR）基因敲除菌株中分别部分和完全恢复。两种菌株的鞭毛蛋白合成和运动性均未恢复。
