Nucleoid-associated proteins shape chromatin structure and transcriptional regulation across the bacterial kingdom

Transcription ◽  
2021 ◽  
pp. 1-37
Author(s):  
Haley M. Amemiya ◽  
Jeremy Schroeder ◽  
Peter L. Freddolino
2010 ◽  
Vol 192 (18) ◽  
pp. 4752-4762 ◽  
Author(s):  
Christopher E. Wozniak ◽  
Fabienne F. V. Chevance ◽  
Kelly T. Hughes

ABSTRACT In Salmonella, there are three classes of promoters in the flagellar transcriptional hierarchy. This organization allows genes needed earlier in the construction of flagella to be transcribed before genes needed later. Four operons (fliAZY, flgMN, fliDST, and flgKL) are expressed from both class 2 and class 3 promoters. To investigate the purpose for expressing genes from multiple flagellar promoters, mutants were constructed for each operon that were defective in either class 2 transcription or class 3 transcription. The mutants were checked for defects in swimming through liquids, swarming over surfaces, and transcriptional regulation. The expression of the hook-associated proteins (FlgK, FlgL, and FliD) from class 3 promoters was found to be important for swarming motility. Both flgMN promoters were involved in coordinating class 3 transcription with the stage of assembly of the hook-basal body. Finally, the fliAZY class 3 promoter lowered class 3 transcription in stationary phase. These results indicate that the multiple flagellar promoters respond to specific environmental conditions and help coordinate transcription with flagellar assembly.


PLoS ONE ◽  
2020 ◽  
Vol 15 (11) ◽  
pp. e0242348
Author(s):  
Ryuta Asada ◽  
Satoshi Senmatsu ◽  
Ben Montpetit ◽  
Kouji Hirota

Chromatin structure, including nucleosome positioning, has a fundamental role in transcriptional regulation through influencing protein-DNA interactions. DNA topology is known to influence chromatin structure, and in doing so, can also alter transcription. However, detailed mechanism(s) linking transcriptional regulation events to chromatin structure that is regulated by changes in DNA topology remain to be well defined. Here we demonstrate that nucleosome positioning and transcriptional output from the fission yeast fbp1 and prp3 genes are altered by excess topoisomerase activity. Given that lncRNAs (long noncoding RNAs) are transcribed from the fbp1 upstream region and are important for fbp1 gene expression, we hypothesized that local changes in DNA topological state caused by topoisomerase activity could alter lncRNA and fbp1 transcription. In support of this, we found that topoisomerase overexpression caused destabilization of positioned nucleosomes within the fbp1 promoter region, which was accompanied by aberrant fbp1 transcription. Similarly, the direct recruitment of topoisomerase, but not a catalytically inactive form, to the promoter region of fbp1 caused local changes in nucleosome positioning that was also accompanied by altered fbp1 transcription. These data indicate that changes in DNA topological state induced by topoisomerase activity could lead to altered fbp1 transcription through modulating nucleosome positioning.


2018 ◽  
Vol 200 (8) ◽  
Author(s):  
Yang Zhang ◽  
Jun Yang ◽  
Guangchun Bai

ABSTRACT Clustered regularly interspaced short palindromic repeats (CRISPR) and the CRISPR-associated proteins (Cas) provide bacteria and archaea with adaptive immunity to specific DNA invaders. Mycobacterium tuberculosis encodes a type III CRISPR-Cas system that has not been experimentally explored. In this study, we found that the CRISPR-Cas systems of both M. tuberculosis and Mycobacterium bovis BCG were highly upregulated by deletion of Rv2837c ( cnpB ), which encodes a multifunctional protein that hydrolyzes cyclic di-AMP (c-di-AMP), cyclic di-GMP (c-di-GMP), and nanoRNAs (short oligonucleotides of 5 or fewer residues). By using genetic and biochemical approaches, we demonstrated that the CnpB-controlled transcriptional regulation of the CRISPR-Cas system is mediated by an Orn-like activity rather than by hydrolyzing the cyclic dinucleotides. Additionally, our results revealed that tuberculosis (TB) complex mycobacteria are functional in processing CRISPR RNAs (crRNAs), which are also more abundant in the Δ cnpB strain than in the parent strain. The elevated crRNA levels in the Δ cnpB strain could be partially reduced by expressing Escherichia coli orn . Our findings provide new insight into transcriptional regulation of bacterial CRISPR-Cas systems. IMPORTANCE Clustered regularly interspaced short palindromic repeats (CRISPR) and the CRISPR-associated proteins (Cas) provide adaptive immunity to specific DNA invaders. M. tuberculosis encodes a type III CRISPR-Cas system that has not been experimentally explored. In this study, we first demonstrated that the CRISPR-Cas systems in tuberculosis (TB) complex mycobacteria are functional in processing CRISPR RNAs (crRNAs). We also showed that Rv2837c (CnpB) controls the expression of the CRISPR-Cas systems in TB complex mycobacteria through an oligoribonuclease (Orn)-like activity, which is very likely mediated by nanoRNA. Since little is known about regulation of CRISPR-Cas systems, our findings provide new insight into transcriptional regulation of bacterial CRISPR-Cas systems.


2011 ◽  
Vol 2011 ◽  
pp. 1-30 ◽  
Author(s):  
Toshiharu Takeda ◽  
Choong-Soo Yun ◽  
Masaki Shintani ◽  
Hisakazu Yamane ◽  
Hideaki Nojiri

Bacterial nucleoid-associated proteins (NAPs) form nucleoprotein complexes and influence the expression of genes. Recent studies have shown that some plasmids carry genes encoding NAP homologs, which play important roles in transcriptional regulation networks between plasmids and host chromosomes. In this study, we determined the distributions of the well-known NAPs Fis, H-NS, HU, IHF, and Lrp and the newly found NAPs MvaT and NdpA among the whole-sequenced 1382 plasmids found in Gram-negative bacteria. Comparisons between NAP distributions and plasmid features (size, G+C content, and putative transferability) were also performed. We found that larger plasmids frequently have NAP gene homologs. Plasmids with H-NS gene homologs had less G+C content. It should be noted that plasmids with the NAP gene homolog also carried the relaxase gene involved in the conjugative transfer of plasmids more frequently than did those without the NAP gene homolog, implying that plasmid-encoded NAP homologs positively contribute to transmissible plasmids.


Genetics ◽  
1995 ◽  
Vol 140 (1) ◽  
pp. 103-114 ◽  
Author(s):  
Y W Jiang ◽  
D J Stillman

Abstract The yeast SIN4 gene functions in the transcriptional activation and repression of diverse yeast genes. Previous experiments suggest a sin4 mutation affects chromatin structure and thus alters transcriptional regulation. In this report we show that SIN4 is required for full expression of the HIS4, Ty1, and MAT alpha genes, in addition to the previously described SIN4-dependence of CTS1 expression. All of these genes contain within their promoters a binding site for the Rap1p transcriptional regulator. However, SIN4 does not play a direct role either in transcriptional activation or repression by Rap1p. The HIS4 gene can be activated by either of two pathways, the basal or the inducible pathway, and experiments are described that show that a sin4 mutation affects both pathways. It was shown previously that mutation of the Rap1p binding site in the HIS4 promoter causes a similar effect on HIS4 expression and that this promoter mutation also causes a change in chromatin structure. The SNF2/SWI2 gene is also required for full HIS4 expression, and we show that a sin4 snf2 double mutant is not synergistic compared to either single mutant. We show that nucleosomes are positioned at the HIS4 promoter and that this positioning is disrupted in a snf2 mutant but not in a sin4 mutant. These findings suggest that SIN4 plays a distinct role in transcriptional regulation.


2020 ◽  
Vol 21 (21) ◽  
pp. 8087
Author(s):  
Maxence Cornut ◽  
Emilie Bourdonnay ◽  
Thomas Henry

Inflammasomes are multimolecular complexes with potent inflammatory activity. As such, their activity is tightly regulated at the transcriptional and post-transcriptional levels. In this review, we present the transcriptional regulation of inflammasome genes from sensors (e.g., NLRP3) to substrates (e.g., IL-1β). Lineage-determining transcription factors shape inflammasome responses in different cell types with profound consequences on the responsiveness to inflammasome-activating stimuli. Pro-inflammatory signals (sterile or microbial) have a key transcriptional impact on inflammasome genes, which is largely mediated by NF-κB and that translates into higher antimicrobial immune responses. Furthermore, diverse intrinsic (e.g., circadian clock, metabolites) or extrinsic (e.g., xenobiotics) signals are integrated by signal-dependent transcription factors and chromatin structure changes to modulate transcriptionally inflammasome responses. Finally, anti-inflammatory signals (e.g., IL-10) counterbalance inflammasome genes induction to limit deleterious inflammation. Transcriptional regulations thus appear as the first line of inflammasome regulation to raise the defense level in front of stress and infections but also to limit excessive or chronic inflammation.


Blood ◽  
1994 ◽  
Vol 83 (7) ◽  
pp. 1822-1830 ◽  
Author(s):  
XY He ◽  
PN Cockerill ◽  
D Cen ◽  
BR Davis

Abstract The human CD34 surface antigen is selectively expressed on stem/progenitor cells within the hematopoietic system. Because CD34 expression is tightly linked to the immature status of hematopoietic cells, with expression being rapidly lost as hematopoietic cells mature and differentiate, an examination of its regulation may provide important insights into the molecular control of blood cell development. A comparison of the CD34 nuclear transcription rate in CD34+ and CD34- cells indicated that the CD34 gene is transcriptionally regulated in hematopoietic cell lines. In a previous report, we had identified two major clusters of CD34 transcription initiation sites by 5′ RACE (rapid amplification of cDNA ends) analysis. In transient transfection experiments, we now demonstrate the ability of sequences encompassing each of these clusters to function as promoters of transcription in CD34+ cells. These promoters functioned at equivalent levels in CD34+ and CD34- cells, and the addition of 5′ flanking sequences, extending as far as 3.7 kb upstream, to the core promoters did not differentially modify the level of expression in CD34+ versus the CD34- cell lines. An examination of DNase I hypersensitivity sites within an 18-kb segment of DNA, extending 9 kb either side of the proximal promoter, showed six sites that were primarily associated with CD34- expressing cells. Taken together, these data indicate that the CD34 promoter sequences alone do not confer tissue-or stage-specific expression. Appropriate transcriptional regulation of the CD34 gene must be controlled by chromatin structure, as identified by DNase I hypersensitivity, and/or by other tissue- and stage-specific elements present outside of the promoter region.


Leukemia ◽  
1999 ◽  
Vol 13 (5) ◽  
pp. 750-759 ◽  
Author(s):  
JL Fordham ◽  
B Göttgens ◽  
F McLaughlin ◽  
AR Green

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