Ding Yanpeng, Davis Brigid M, Waldor Matthew K
Howard Hughes Medical Institute and Tufts University School of Medicine, 136 Harrison Ave., Boston, MA 02111, USA.
Mol Microbiol. 2004 Jul;53(1):345-54. doi: 10.1111/j.1365-2958.2004.04142.x.
Hfq is an RNA-binding protein that interacts with both small untranslated RNAs (sRNAs) and mRNAs to modulate gene expression post-transcriptionally. In Escherichia coli and Salmonella typhimurium, Hfq is required for efficient expression of the stationary phase sigma factor sigma(S), and consequently is critical for Salmonella virulence. We have found that Hfq is also essential for the virulence of Vibrio cholerae, as strains lacking hfq fail to colonize the suckling mouse intestine. Deletion of the V. cholerae hfq does not prevent production of sigma(S), nor does it prevent expression of TCP, V. cholerae's primary colonization factor. The expression and activity of the alternative sigma factor sigma(E) are dramatically increased in a V. cholerae hfq mutant. Comparison of the transcriptome of an hfq mutant with that of an rseA mutant, which also overexpresses sigma(E), revealed that sigma(E) controls approximately half the genes found to be upregulated in the hfq mutant. However, increased sigma(E) does not appear to account for this strain's reduced virulence. It is likely that sRNAs, in conjunction with Hfq, are critical regulators of V. cholerae pathogenicity.
Hfq是一种RNA结合蛋白，它与小非编码RNA（sRNA）和mRNA相互作用，在转录后调节基因表达。在大肠杆菌和鼠伤寒沙门氏菌中，Hfq是稳定期σ因子σ（S）高效表达所必需的，因此对沙门氏菌的毒力至关重要。我们发现，Hfq对霍乱弧菌的毒力也至关重要，因为缺乏hfq的菌株无法在乳鼠肠道中定殖。霍乱弧菌hfq的缺失并不阻止σ（S）的产生，也不阻止霍乱弧菌主要定殖因子TCP的表达。在霍乱弧菌hfq突变体中，替代σ因子σ（E）的表达和活性显著增加。将hfq突变体的转录组与同样过表达σ（E）的rseA突变体的转录组进行比较，发现σ（E）控制着在hfq突变体中上调的约一半基因。然而，σ（E）的增加似乎并不能解释该菌株毒力的降低。sRNA与Hfq结合，很可能是霍乱弧菌致病性的关键调节因子。
