In the plant pathogen Streptomyces scabies, the gene bglC encodes a GH1 family cellobiose beta-glucosidase that is both required for primary metabolism and for inducing virulence of the bacterium. Deletion of bglC (strain ΔbglC) surprisingly resulted in the augmentation of the global beta-glucosidase activity of S. scabies. This paradoxical phenotype is highly robust as it has been observed in all bglC deletion mutants independently generated, thereby highlighting a phenomenon of genetic compensation. Comparative proteomics allowed to identify two glycosyl hydrolases – named BcpE1 and BcpE2 – of which peptide levels were significantly increased in strain ΔbglC. Quantitative RT-PCR revealed that the higher abundance of BcpE1 and BcpE2 is triggered at the transcriptional level, the expression of their respective gene being 100 and 15 times upregulated. Enzymatic studies with pure BcpE proteins showed that they both possess beta-glucosidase activity thereby explaining the genotypic-phenotypic discrepancy of the bglC deletion mutant. The GH1 family BcpE1 could hydrolyze cellobiose and generate glucose similarly to BglC itself thereby mainly contributing to the survival of strain ΔbglC when cellobiose is provided as sole nutrient source. The low affinity of BcpE2 for cellobiose suggests that this GH3 family beta-glucosidase would instead primarily target another and yet unknown glucose-beta-1,4-linked substrate. These results make S. scabies a new model system to study genetic compensation. Discovering how, either the bglC DNA locus, its mRNA, the BglC protein, or either its enzymatic activity controls bcpE genes' expression, will unveil new mechanisms directing transcriptional repression.

在植物病原体链霉菌sc疮中，基因bglC编码一个GH1家族纤维二糖β-葡萄糖苷酶，这既是初级代谢又是诱导细菌毒性所必需的。bglC（菌株ΔbglC）的删除令人惊讶地导致了sc疮。的整体β-葡糖苷酶活性的增加。这种矛盾的表型具有很强的鲁棒性，因为在所有独立产生的bglC缺失突变体中均已观察到，从而突显了遗传补偿现象。比较蛋白质组学可以鉴定出两个糖基水解酶（分别称为BcpE1和BcpE2），其中的肽水平在菌株ΔbglC中显着增加。定量RT-PCR显示，在转录水平上触发了更高的BcpE1和BcpE2丰度，它们各自基因的表达被上调了100和15倍。用纯BcpE蛋白进行的酶学研究表明，它们都具有β-葡萄糖苷酶活性，从而可以解释bglC缺失突变体的基因型-表型差异。GH1家族BcpE1可以像BglC本身一样水解纤维二糖并产生葡萄糖，从而当提供纤维二糖作为唯一的营养源时，主要有助于菌株ΔbglC的存活。BcpE2对纤维二糖的低亲和力表明，该GH3家族的β-葡萄糖苷酶将主要针对另一种未知的葡萄糖-β-1,4连接的底物。这些结果使S.ies疮研究遗传补偿的新模型系统。发现bglC DNA基因座，其mRNA，BglC蛋白或其酶活性如何控制bcpE基因的表达，将揭示指导转录抑制的新机制。