However, PD 0332991 CDK inhibitor although the ybjN expression levels are positively correlated to ability of the ts9 mutant to survive at high temperatures, the ICG-001 mutation of the ybjN itself did not result in temperature sensitivity, and growth of the ybjN mutant is similar to that of the BW strain. These results indicate that decreased ybjN expression in the ts9 mutant alone may not directly contribute to its temperature sensitivity, but over-expression of ybjN is required for its ability to grow at higher temperature. We still do not know why mutations in the ts9 strain result in the reductions in ybjN expression levels. Our microarray results may have shed some light on solving the mysteries of the above mentioned phenomenon. We demonstrated that over-expression of ybjN led to significant down-regulation of genes involved in metabolism, but promotion of stress-related gene expression such as the toxin-antitoxin modules, the SOS stress response, cold shock and phage-shock genes. This expression pattern is very similar to those reported for so-called persister cells. Persister cells are dormant variants of normal bacterial cells and are highly tolerant to antibiotics. Transcriptome studies of persister cells have revealed down-regulation of biosynthesis genes and increased expression of toxin/antitoxin modules, SOS response and cold shock genes. A recent study reported that MqsR promotes formation of persister cells through activation of the cold shock protein CpsD. It has also been reported that over-expression of the RelE toxin, an inhibitor of translation, results in cellular function shut-down and a sharp increase in persisters. On the contrary, deletion of the hipA gene decreases in persister formation in both stationary and biofilm populations. In this study, ybjN over-expression strains may also induce a dormancy state similar to that of persister cells, which leads to growth slowdown as well as phenotypic switch to a state similar to that of persistence. Several independent studies have revealed that autoaggregation has an inverse correlation with flagellar and fimbriae production. Expression of autoaggregation factor antigen 43 and genes involved in flagellation and fimbriation are mutually exclusive. Moreover, autoaggregation strains caused by overproduction of antigen 43 are deficient in bacterial appendage production. In this study, it has been demonstrated that ybjN over-expression mediated-autoaggregation down-regulated flagellar and fimbrial gene expression, hence resulting in reduced motility and fimbriation. In contrast, a mutation in ybjN led to over production of flagella and fimbriae, thus increasing motility and fimbriation, and indicating that YbjN is a negative regulator of flagellar and fimbriae biosynthesis. However, antigen 43 is not upregulated in the ybjN over-expression strain, suggesting that YbjN��s effect on autoaggregation is independent of the antigen 43 pathway.