de la Peña-Moctezuma A, Bulach D M, Adler B
Bacterial Pathogenesis Research Group, Department of Microbiology, Monash University 3800, Clayton, Vic., Australia.
FEMS Immunol Med Microbiol. 2001 Jul;31(1):73-81. doi: 10.1111/j.1574-695X.2001.tb01589.x.
The gene organization in the lipopolysaccharide biosynthetic (rfb) locus was analyzed in seven Leptospira interrogans serovars within serogroup Icterohemorrhagiae, seven non-Icterohemorrhagiae serovars and one Leptospira borgpetersenii serovar. Two groups of loci were delineated based on DNA hybridization and sequence analysis. Group 1 contained the two Hardjo subtypes, Hardjoprajitno and Hardjobovis. Group 2 (containing Copenhageni, Pomona, Naam, Mwogolo, Smithi, Lai, Canicola, Autumnalis, Pyrogenes, Australis and Icterohemorrhagiae) differed from Group 1 in its organization upstream of orf11, where five ORFs (32, 33, 34, 35, 37) were identified that were not contained in the Group 1 loci. These ORFs encoded a putative epimerase (orf32), a glycosyltransferase (orf33), two integral membrane proteins (orfs 34 and 35), and a galactosyltransferase (orf37). Serovars Australis, Pomona and Autumnalis did not contain orf37. Serovar Bataviae was excluded from the grouping because of its unique genetic organization upstream of orf13. In the Group 2 loci, comparison of the genetic layout at the 5' end revealed differences which included mutations disrupting reading frames in either or both orf34 and orf35 and apparent allelic differences between orf33 homologs that may be sufficient to account for the genetic basis of serovar identity.
对出血热群中的7个问号钩端螺旋体血清型、7个非出血热血清型和1个博氏钩端螺旋体血清型的脂多糖生物合成（rfb）基因座中的基因组织进行了分析。基于DNA杂交和序列分析确定了两组基因座。第1组包含两个哈焦亚型，即哈焦普拉吉特诺型和哈焦波维斯型。第2组（包含哥本哈根型、波摩那型、那姆型、姆沃戈洛型、史密氏型、赖型、犬型、秋季热型、热解型、澳洲型和出血热型）在orf11上游的组织与第1组不同，在第2组基因座中鉴定出了5个ORF（32、33、34、35、37），而第1组基因座中没有这些ORF。这些ORF编码一种假定的表异构酶（orf32）、一种糖基转移酶（orf33）、两种整合膜蛋白（orf34和orf35）和一种半乳糖基转移酶（orf37）。澳洲型、波摩那型和秋季热型血清型不包含orf37。由于巴氏血清型在orf13上游具有独特的基因组织，因此被排除在分组之外。在第2组基因座中，5'端基因布局的比较揭示了差异，其中包括破坏orf34和orf35一个或两个阅读框的突变，以及orf33同源物之间明显的等位基因差异，这些差异可能足以解释血清型同一性的遗传基础。
