Sequence-Based Analysis Uncovers an Abundance of Non-Coding RNA in the Total Transcriptome of Mycobacterium tuberculosis

Arnvig, Kristine B.; Comas, Iñaki; Thomson, Nicholas R.; Houghton, Joanna; Boshoff, Helena I.; Croucher, Nicholas J.; Rose, Graham; Perkins, Timothy T.; Parkhill, Julian; Dougan, Gordon; Young, Douglas B.

doi:10.1371/journal.ppat.1002342

Cited by 220 publications

(456 citation statements)

References 75 publications

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“…Calculation of pairwise correlation coefficients demonstrated a high degree of reproducibility between this dataset (Spearman r ranging from 0.80 to 0.85; see Fig. S1, available in the online Supplementary Material) and previously published transcriptome analyses of exponentially growing M. tuberculosis by RNaseq (Arnvig et al, 2011;Cortes et al, 2013). …”

Section: Methodssupporting

confidence: 55%

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Transcription and translation of the rpsJ, rplN and rRNA operons of the tubercle bacillus

Cortes¹,

Cox²

2015

Microbiology

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Several species of the genus Mycobacterium are human pathogens, notably the tubercle bacillus (Mycobacterium tuberculosis). The rate of proliferation of a bacterium is reflected in the rate of ribosome synthesis. This report describes a quantitative analysis of the early stages of the synthesis of ribosomes of M. tuberculosis. Specifically, the roles of three large operons, namely: the rrn operon (1.7 microns) encoding rrs (16S rRNA), rrl (23S rRNA) and rrf (5S rRNA); the rpsJ operon (1.93 microns), which encodes 11 ribosomal proteins; and the rplN operon (1.45 microns), which encodes 10 ribosomal proteins. A mathematical framework based on properties of population-average cells was developed to identify the number of transcripts of the rpsJ and rplN operons needed to maintain exponential growth. The values obtained were supported by RNaseq data. The motif 59-gcagac-39 was found close to 59 end of transcripts of mycobacterial rplN operons, suggesting it may form part of the RpsH feedback binding site because the same motif is present in the ribosome within the region of rrs that forms the binding site for RpsH.

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Section: Methodssupporting

confidence: 55%

“…M. tuberculosis H37Rv was grown in Middlebrook 7H9 medium supplemented with 0.2 % w/v glycerol and 10 % Albumin Dextrose Catalase (ADC) supplement in roller bottle culture. RNA was isolated from mid-exponentially growing bacteria as described by Arnvig et al (2011). RNA was treated with Turbo DNase (Ambion) until DNA free.…”

Section: Methodsmentioning

confidence: 99%

Transcription and translation of the rpsJ, rplN and rRNA operons of the tubercle bacillus

Cortes¹,

Cox²

2015

Microbiology

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“…Thus, several dozen toxins encoded by the Mtb genome contain the potential to target and degrade specific transcripts and are regulated by their cognate antitoxin pairs yet exhibit promiscuous binding affinities (35,36). Numerous small RNA molecules with the ability to disrupt gene expression have been identified (37).…”

Section: Discussionmentioning

confidence: 99%

The Mycobacterium tuberculosis Clp Gene Regulator Is Required for in Vitro Reactivation from Hypoxia-induced Dormancy

McGillivray

Golden

Kaushal

2015

Journal of Biological Chemistry

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“…In particular, there is a growing area of research into the roles of nucleoid-associated proteins and small RNAs (150)(151)(152)(153)(154)(155). M. tuberculosis also contains 11 serine/ threonine protein kinases (STPKs) that, like TCSs, are involved in signal transduction pathways that aid M. tuberculosis in adaptation to its environment (156 …”

Section: Final Thoughtsmentioning

confidence: 99%

Mycobacterium tuberculosis Transcription Machinery: Ready To Respond to Host Attacks

2016

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Regulating responses to stress is critical for all bacteria, whether they are environmental, commensal, or pathogenic species. For pathogenic bacteria, successful colonization and survival in the host are dependent on adaptation to diverse conditions imposed by the host tissue architecture and the immune response. Once the bacterium senses a hostile environment, it must enact a change in physiology that contributes to the organism's survival strategy. Inappropriate responses have consequences; hence, the execution of the appropriate response is essential for survival of the bacterium in its niche. Stress responses are most often regulated at the level of gene expression and, more specifically, transcription. This minireview focuses on mechanisms of regulating transcription initiation that are required by Mycobacterium tuberculosis to respond to the arsenal of defenses imposed by the host during infection. In particular, we highlight how certain features of M. tuberculosis physiology allow this pathogen to respond swiftly and effectively to host defenses. By enacting highly integrated and coordinated gene expression changes in response to stress, M. tuberculosis is prepared for battle against the host defense and able to persist within the human population.T he survival of any organism relies on its ability to sense and respond to changes in its environment. For bacteria, stress responses are primarily mediated through the regulation of gene expression. By integrating multiple molecular approaches to gene regulation, pathogenic bacteria are able to orchestrate conditionspecific patterns that promote survival and pathogenesis in the face of a strong immune response. This minireview focuses on mechanisms of transcription regulation required for stress responses in one of the most successful and deadly pathogens in the world, Mycobacterium tuberculosis. M. tuberculosis has coexisted with humans for Ͼ50,000 years (1) and continues to cause more than 1.5 million deaths a year (2). The coevolution of M. tuberculosis with the human host response to infection has resulted in a pathogen that is specialized for long-term infection in people. Tuberculosis is a complex disease that requires the bacteria to multiply within phagocytes, survive extracellularly in hypoxic and necrotic granulomas, and endure a robust immune response to persist in the host. During infection, the host immune response restrains M. tuberculosis from proliferating by imposing a battery of defenses, including reactive oxygen and nitrogen stress, hypoxia, acid stress, genotoxic stress, cell surface stress, and starvation (3). Despite this onslaught of attacks, M. tuberculosis is able to persist for the lifetime of the host, indicating that this pathogen has highly effective molecular mechanisms to resist host-inflicted damage. In order to enact these defenses and facilitate this specialized lifestyle, M. tuberculosis executes a complex, interconnected web of stress responses that rely on changes in gene expression. In fact, M. tuberculosis is well suite...

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Sequence-Based Analysis Uncovers an Abundance of Non-Coding RNA in the Total Transcriptome of Mycobacterium tuberculosis

Cited by 220 publications

References 75 publications

Transcription and translation of the rpsJ, rplN and rRNA operons of the tubercle bacillus

Transcription and translation of the rpsJ, rplN and rRNA operons of the tubercle bacillus

The Mycobacterium tuberculosis Clp Gene Regulator Is Required for in Vitro Reactivation from Hypoxia-induced Dormancy

Mycobacterium tuberculosis Transcription Machinery: Ready To Respond to Host Attacks

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