Project description:The natural biotope of Bacillus subtilis is the upper layer of soil where it grows as a biofilm. To mimic this physiological development and study the impact of nanoparticles during the formation of a biofilm in a contaminated soil, we have studied the proteomic response of the ancestral strain Bacillus subtilis 3610, which is able to form biofilm contrary to the 168 laboratory strain. The bacteria were grown on soft agar plates containing n-ZnO, n-TiO2 or ZnSO4 metal ion.
Project description:Transcriptional profiling of Bacillus subtilis str 3610 cells comparing sinR-/epsH- cells to sinR-/epsH-/remA- cells in MSgg Medium at optical density (600nm) of 1.0
Project description:In our study, we found that lack of tmRNA affects the biofilm formation in Bacillus subtilis, which has important research significance. Then, we obtained a revertant strain MB from tmRNA mutant strain. And MB strain could restore biofilm production capacity. Therefore, the transcriptomes of the three strains were sequenced. Based on the statistical analysis of gene expression (P < 0.05), there were 756 genes up regulated while 992 genes down regulated by at least two folds when comparing TM to WT. Secondly, there were 974 genes up regulated while 563 genes down regulated by at least two folds when comparing MB to TM. And there were 179 genes up regulated while 307 genes down regulated by at least two folds when comparing MB to WT.
Project description:RNA-DNA hybrids form throughout the chromosome during normal cell growth and under stress conditions. When left unresolved, RNA-DNA hybrids can slow replication fork progression, cause DNA breaks, increase mutagenesis, and reduce gene expression. To remove hybrids, all organisms use ribonuclease H (RNase H) to specifically degrade the RNA portion of RNA-DNA hybrids. Here we show that, in addition to chromosomally encoded RNase HII and RNase HIII, Bacillus subtilis NCIB 3610 encodes a previously uncharacterized RNase HI protein, RnhP, on the endogenous plasmid pBS32. Like other RNase HI enzymes, RnhP incises Okazaki fragments, ribopatches, and a complementary RNA-DNA hybrid. We show that while chromosomally encoded RNase HIII is required for pBS32 hyper-replication, RnhP compensates for loss of RNase HIII activity on the chromosome. Consequently, loss of RnhP and RNase HIII impairs bacterial growth. We show that the decreased growth rate can be explained by laggard replication fork progression near the terminus region of the right replichore resulting in SOS-dependent inhibition of cell division. We conclude that B. subtilis NCIB 3610 encodes functional RNase HI, HII, and HIII, and pBS32-encoded RNase HI contributes to replication fork progression and chromosome stability while RNase HIII is important for chromosome stability and plasmid hyper-replication.
Project description:RNA-DNA hybrids form throughout the chromosome during normal cell growth and under stress conditions. When left unresolved, RNA-DNA hybrids can slow replication fork progression, cause DNA breaks, increase mutagenesis, and reduce gene expression. To remove hybrids, all organisms use ribonuclease H (RNase H) to specifically degrade the RNA portion of RNA-DNA hybrids. Here we show that, in addition to chromosomally encoded RNase HII and RNase HIII, Bacillus subtilis NCIB 3610 encodes a previously uncharacterized RNase HI protein, RnhP, on the endogenous plasmid pBS32. Like other RNase HI enzymes, RnhP incises Okazaki fragments, ribopatches, and a complementary RNA-DNA hybrid. We show that while chromosomally encoded RNase HIII is required for pBS32 hyper-replication, RnhP compensates for loss of RNase HIII activity on the chromosome. Consequently, loss of RnhP and RNase HIII impairs bacterial growth. We show that the decreased growth rate can be explained by laggard replication fork progression near the terminus region of the right replichore resulting in SOS-dependent inhibition of cell division. We conclude that B. subtilis NCIB 3610 encodes functional RNase HI, HII, and HIII, and pBS32-encoded RNase HI contributes to replication fork progression and chromosome stability while RNase HIII is important for chromosome stability and plasmid hyper-replication.
