RNase Y is responsible for uncoupling the expression of translation factor IF3 from that of the ribosomal proteins L35 and L20 in Bacillus subtilis.

RNase Y is a novel endoribonuclease affecting global mRNA metabolism. We show that this nuclease affects the expression of the Bacillus subtilis infC-rpmI-rplT operon, encoding translation initiation factor IF3 and the ribosomal proteins L35 and L20. This operon is autoregulated by a complex L20-dependent transcription attenuation mechanism. L20 binds to a phylogenetically conserved domain on the 5' untranslated region of the infC mRNA which mimics the L20 binding sites on 23S rRNA. We have identified a second promoter (P1) upstream of the previously identified promoter (P2). The P1, but not the P2, readthrough transcript is stabilized in a strain depleted for RNase Y. However, under these conditions infC biosynthesis is repressed threefold. We show that the unprocessed P1 transcript is non-functional for IF3 translation but fully competent to express the co-transcribed ribosomal protein genes. RNase Y cleavage of the P1 transcript creates an entry site for the 5'-3' exonucleolytic activity of RNase J1 which degrades the infC mRNA when translation initiation efficiency is low. A second RNase Y cleavage is crucial for initiating degradation of the prematurely terminated infC leader RNAs, including the L20 operator complex, which permits efficient recycling of the L20 protein.

[Expression change of TIF3 p36 at different stages of human bronchial epithelial cells transformed and induced by cadmium chloride].

OBJECTIVE: To explore the molecular mechanisms potentially responsible for carcinogenesis due to cadmium by detecting expression change of the translation initiation factor 3 (TIF3 p36) in those malignant transformation of human bronchial epithelial cell lines (16HBE) induced by cadmium chloride (CdCl(2)). METHODS: The expression changes of TIF3 p36 were detected and analyzed at different stages of malignant cells (semi transformed cells, transformed cells and tumorigenic cells) induced by CdCl(2) solution with both reverse transcription PCR technique and sensitive fluorescent quantitative PCR assay. RESULTS: Compared with non-transformed human bronchial epithelial cells, the results of fluorescent quantitative PCR assay showed that the semi-transformed cells, transformed cells and tumorigenic cells all expressed higher levels of TIF3 p36 mRNA (P < 0.01 or P < 0.05). As compared with the control cells, the TIF3 expressions at different stages of malignant transformation were 3.1 times, 5.9 times and 9.9 times higher respectively in the low dosage group of CdCl(2) (5 micromol/L); 7.1 times, 6.8 times and 14.8 times respectively in the middle dosage group of CdCl(2) (10 micromol/L); 3.6 times, 3.0 times and 9.1 times respectively in high of dose of CdCl(2) (15 micromol/L). These results showed that there was the positive correlation between overexpression levels of TIF3 p36 mRNA and the malignant degree of the cells, but they were not related to the dosages of cadmium. CONCLUSION: There is significantly abnormal overexpression of TIF3 gene during malignant transformation of human bronchial epithelial cell line induced by cadmium chloride, and the TIF3 expression is associated with the malignant degree of the cells, which may be one of molecular mechanisms potentially responsible for the carcinogenesis due to cadmium.