Energetics of Respiration and Oxidative Phosphorylation in Mycobacteria

In the paper

“In M. tuberculosis, the bc1-aa3 pathway is essential for growth suggesting an inability of this bacterium to adapt in a manner analogous to M. smegmatis (70).”

What the sources say

• Disputed

  The Discussion describes the pathway’s essentiality in M. tuberculosis as apparent, based on failure to recover mutants under the conditions tested. Although it considers inability to adapt as a possibility, it concludes that respiratory adaptation probably does occur in M. tuberculosis; the mutants may instead grow too poorly to be detected. (LLM, conf=0.88)

  Checked by a reasoning model — may be wrong.

  cites [70] sourceExperimental — accuracy not yet measured

In the paper

“Several studies have reported that nuo is down-regulated in M. tuberculosis during mouse lung infection (18), survival in macrophages (19), in both non-replicating persistence (NRP)-1 (1% oxygen saturation) and NRP-2 (0.06% oxygen saturation) relative to aerated mid-log growth (18), and upon starvation in vitro (20).”

What the sources say

• Supported

  The source reports decreased nuoB transcripts during mouse lung infection in Results and Discussion and a 3- and 6-fold decrease in NRP-1 and NRP-2, respectively, relative to aerated mid-log growth in “A Model of M. tuberculosis Respiratory Flexibility During Infection.” The macrophage-survival and starvation clauses have separate citations in the citing sentence and are not attributed to this source. (LLM, conf=0.94)

  cites [18] source
• Supported

  The “Energy Production During Anaerobic Respiration” section reports that genes encoding NADH dehydrogenase 1 (nuoABDFIL) were repressed in intraphagosomal M. tuberculosis relative to logarithmically growing bacteria. This supports the macrophage portion of the citing sentence, which is the portion attributed to this paper; the other conditions have separate citations. No page number is available in our copy. (LLM, conf=0.94)

  cites [19] source
• Supported

  The citation to this paper is attached to the in vitro starvation portion of the sentence, not the mouse, macrophage, or NRP conditions. The Energy metabolism section (pp. 717–731) reports that the nuoA–M operon is downregulated in the nutrient-starvation model. (LLM, conf=0.94)

  cites [20] source

In the paper

“Proline dehydrogenase is upregulated under both energy-limiting conditions and hypoxia (7, 16)”

What the sources say

• ?Not checked — no full text of the sourcecites [7] source
• Partly supported

  The Results (Energy Metabolism; page unavailable) identify proline dehydrogenase as upregulated during energy-limited slow growth. The same section says that nearly all dehydrogenases upregulated during slow growth had very low mRNA levels under hypoxia, with hydrogenases the only exceptions. It therefore does not support the claim that proline dehydrogenase was also upregulated under hypoxia. (LLM, conf=0.90)

  cites [16] sourceExperimental — accuracy not yet measured

In the paper

“Gene expression studies suggest that Hyd1 and Hyd2 are used during nutrient starvation as an alternative electron source (Figure 2) while Hyd3 and the membrane-bound hydrogenase are more likely to have a function in disposing electrons under anaerobic conditions (16) (Figure 3).”

What the sources say

• Partly supported

  The Results (Energy Metabolism; page unavailable) show that Hyd3 is upregulated under low oxygen, and the Discussion (Adaptation to Hypoxia; page unavailable) proposes hydrogen production as a redox sink under hypoxia. But the paper predicts all three hydrogenases to be soluble, not membrane-bound, and does not establish electron disposal as Hyd3’s specific function. (LLM, conf=0.88)

  cites [16] sourceExperimental — accuracy not yet measured

In the paper

“Hyd2 appears to be a founding member of the Group 5 high-affinity hydrogenases (52, 53).”

What the sources say

• ?Could not verify

  The Discussion (p. 6) defines group 5 as a distinct group of putative high-affinity [NiFe]-hydrogenases. Searches for “Hyd2,” “hydrogenase 2,” and a founding member found no passage identifying Hyd2 or placing it in that group, so our copy does not establish the claim about Hyd2. (LLM, conf=0.72)

  cites [52] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [53] source

In the paper

“Hyd1 aligns closely with Group 2a uptake hydrogenases of the cyanobacteria such as Nostoc, indicating it oxidises H2 (51).”

What the sources say

• Partly supported

  The Introduction (page not available) places cyanobacterial uptake hydrogenases in group 2, and the H₂-production section says these enzymes oxidize H₂. The paper does not identify Hyd1 or report its alignment with cyanobacterial hydrogenases, so it does not establish that Hyd1 itself oxidizes H₂. (LLM, conf=0.86)

  cites [51] sourceExperimental — accuracy not yet measured

In the paper

“A more recent study suggests that the glyoxylate shunt, and not the reverse TCA, is used to metabolize both glycolytic and fatty acid carbon sources in response to oxygen limitation and this route also produces succinate as its metabolic end product (43).”

What the sources say

• Supported

  The Discussion states that the study identified the glyoxylate shunt as a pathway capable of metabolizing both glycolytic and fatty-acid carbon sources under oxygen limitation, producing succinate as an end product. The section on succinate-mediated maintenance of membrane potential explicitly contrasts ICL-mediated succinate production with production through the reverse TCA cycle. (LLM, conf=0.94)

  cites [43] source

In the paper

“NDH-2 has not been reported in mammalian mitochondria leading to the proposal that these enzymes may represent a potential drug target for the treatment of human pathogens (6, 12, 27, 30, 31) and intracellular parasites (32).”

What the sources say

• ?Not checked — no full text of the sourcecites [6] source
• Supported

  The Discussion (page unavailable) states that human mitochondria use only type I NADH dehydrogenase and calls type II NADH dehydrogenase an important antimicrobial target. This supports the claim that NDH-2 is absent from mammalian mitochondria and has been proposed as a drug target. (LLM, conf=0.93)

  cites [12] source
• Supported

  The introductory passage (page unavailable) says NDH-2 is not found in mitochondria and describes it as essential to M. tuberculosis. The same section reports that phenothiazines inhibit NDH-2 and hinder M. tuberculosis growth, supporting the proposal that it may be a drug target. The paper does not establish that absence for every kind of mitochondrion; the citing claim is limited to mammalian mitochondria. (LLM, conf=0.87)

  cites [27] source

In the paper

“The second class is NDH-2, a non-proton translocating type II NADH dehydrogenase that does not conserve energy and is present in two copies (Ndh and NdhA) in M. tuberculosis (12) (Table 1).”

What the sources say

• Supported

  The Results section describes M. tuberculosis NDH-2 as a nonproton-pumping oxidoreductase present in two copies, ndh and ndhA. In this enzyme-level context, nonproton-pumping supports the characterization that NDH-2 does not conserve energy through proton translocation. (LLM, conf=0.90)

  cites [12] source

In the paper

“The authors propose that during oxygen limitation large amounts of succinate are produced by this pathway that are used to sustain the membrane potential, ATP synthesis and TCA cycle precursors akin to a “metabolic battery” (43).”

What the sources say

• Supported

  The Discussion states that, as oxygen is depleted, M. tuberculosis increases glyoxylate-shunt activity, produces large amounts of succinate, and can use it to sustain membrane potential, ATP synthesis, and anaplerosis depending on conditions. It also describes succinate as a multifunctional “metabolic battery” that sustains TCA cycle precursors. (LLM, conf=0.94)

  cites [43] source

In the paper

“It has been shown that M. smegmatis can grow on proline as the sole carbon and energy source and also that PRODH is an important electron donor, under both energy-limiting conditions and hypoxia (7, 16).”

What the sources say

• ?Not checked — no full text of the sourcecites [7] source
• Partly supported

  The Results > Energy Metabolism section (page unavailable) reports that proline dehydrogenase was among the proposed electron donors upregulated during slow growth under energy limitation. It does not establish that M. smegmatis grows on proline as its sole carbon and energy source or that PRODH is an important electron donor under hypoxia; the same section says nearly all dehydrogenases upregulated during slow growth had very low mRNA levels under hypoxia, except hydrogenases. (LLM, conf=0.87)

  cites [16] sourceExperimental — accuracy not yet measured

In the paper

“In fact, SDH1 and SDH2 have been shown to be differentially expressed under energy- or oxygen-limiting conditions in M. smegmatis (16). Under energy-limiting conditions SDH1 was upregulated 4-fold while SDH2 was downregulated 3-fold. Under oxygen-limiting conditions, SDH1 was downregulated 30-fold while SDH2 was upregulated 2-fold.”

What the sources say

• Partly supported

  Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [16] sourceExperimental — accuracy not yet measured

In the paper

“Weinstein et al. identified genes for two classes of NADH:menaquinone oxidoreductases in the genome of M. tuberculosis (12) (Table 1).”

What the sources say

• Supported

  The Results section states that the authors identified two types of NADH dehydrogenase in the M. tuberculosis genome: the 14-subunit NDH-1 encoded by nuoABCDEFGHIJKLMN and NDH-2 present in two copies, ndh and ndhA. This directly supports the attributed identification. (LLM, conf=0.94)

  cites [12] source

In the paper

“It has been shown that M. smegmatis, among other mycobacterial species, can oxidize molecular hydrogen in the presence of carbon monoxide (CO), implying that M. smegmatis expresses a functional hydrogenase (54).”

What the sources say

• Partly supported

  The Results report H₂ uptake by M. smegmatis, supporting the inference that it has a functional hydrogen-oxidizing enzyme. They report CO uptake separately, however, and do not establish that H₂ oxidation occurred in the presence of CO; the paper does not directly identify a hydrogenase. (LLM, conf=0.84)

  cites [54] sourceExperimental — accuracy not yet measured

In the paper

“The membrane-associated malate quinone oxidoreductase (MQO) oxidizes malate to oxaloacetate and transfers the reducing equivalents to menaquinone (MK) (59, 60) (Figure 3).”

What the sources say

• ?Not checked — no full text of the sourcecites [59] source
• Partly supported

  The introductory passage and the L-malate oxidation section state that Mqo oxidizes malate to oxaloacetate and donates electrons at the quinone pool; the latter section demonstrates reduction of ubiquinone-1. The paper does not establish menaquinone specifically as the electron acceptor: it says the natural direct acceptor is most likely a quinone, while menaquinone-4 did not stimulate activity in the reported assay. No page number is available in our copy. (LLM, conf=0.86)

  cites [60] sourceExperimental — accuracy not yet measured

In the paper

“TMC207 is bactericidal towards most species of mycobacteria (109), but is only bacteriostatic against M. avium (118) and M. smegmatis (Berney and Cook, unpublished data).”

What the sources say

• Partly supported

  The Chemistry and in vitro anti-mycobacterial activity section reports bactericidal activity against M. tuberculosis and low MICs for several other mycobacterial species. Low MICs do not establish that the drug is bactericidal against most species. The M. avium and M. smegmatis clauses cite different sources, so they are not judged against this paper; page numbers are unavailable in our copy. (LLM, conf=0.88)

  cites [109] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [118] source

In the paper

“However, a subsequent study has reported that the nirA gene is misannotated and is in fact sirA, a sulfite reductase shown to be essential for growth on sulfate or sulfite as the sole sulfur source (93) (Table 1).”

What the sources say

• Supported

  The Abstract identifies sirA as a sulfite reductase originally misannotated nirA and states that its deletion prevents growth on sulfate or sulfite as the sole sulfur source. The Results specify that this growth finding comes from a Mycobacterium smegmatis deletion mutant. (LLM, conf=0.94)

  cites [93] source

In the paper

“The most promising compounds clinically, the diarylquinolines, have been shown to target the F1Fo-ATP synthase and inhibit ATP synthesis (109, 111, 112).”

What the sources say

• Partly supported

  The Chemistry and in vitro anti-mycobacterial activity section identifies the F0 subunit of ATP synthase as the target of the diarylquinoline R207910 and says the drug inhibits its proton pump. The Discussion says ATP synthase inhibition may lead to ATP depletion, but does not establish direct inhibition of ATP synthesis; nor does the paper rank diarylquinolines as the most promising compounds clinically. Page numbers are unavailable in our copy. (LLM, conf=0.84)

  cites [109] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [111] source
• Supported

  The introduction (p. 2) identifies the diarylquinoline lead compound R207910 as being in Phase IIb clinical trials and says it specifically targets the c-subunit of F1F0-ATP synthase. The study summary (p. 2) reports that R207910 blocks ATP synthase activity, while the p. 3 passage describes inhibition of ATP synthesis and ATP depletion. (LLM, conf=0.91)

  cites [112] source

In the paper

“In M. tuberculosis, cytochrome bd is upregulated in the early stages of NRP-1 (i.e. decreasing oxygen) (68), in NRP-2 (18) and in response to nitric oxide (NO) (18).”

What the sources say

• ?Not checked — no full text of the sourcecites [68] source
• Supported

  The citation to this paper is attached to NRP-2 and nitric oxide, not early NRP-1, which has a separate citation. In “A Model of M. tuberculosis Respiratory Flexibility During Infection,” the paper reports that bd-type oxidase genes were upregulated under both NRP-2 and NO treatment; the provided passages do not give page numbers. (LLM, conf=0.93)

  cites [18] source

In the paper

“Sohaskey (91) has reported that exogenously supplied nitrate has no effect on long-term persistence during gradual oxygen depletion, but played an important role during rapid adaptation to hypoxia (< 18 h).”

What the sources say

• Partly supported

  The Results report that nitrate had no effect on survival during gradual oxygen depletion and improved survival after sudden anaerobiosis. However, the <18 h threshold describes how quickly anaerobic conditions were created, not how long hypoxia lasted; survival was tracked for 26 days. (LLM, conf=0.85)

  cites [91] sourceExperimental — accuracy not yet measured

In the paper

“In contrast, fumarate reductase, nitrate reductase and NDH-2 are all upregulated under these conditions (19).”

What the sources say

• Supported

  The Energy Production During Anaerobic Respiration section states that frdA, narX, and ndh—encoding fumarate reductase, nitrate reductase, and NDH-2—were induced in intraphagosomal M. tuberculosis. The paper specifies that narX induction occurred only in activated macrophages. (LLM, conf=0.91)

  cites [19] source

In the paper

“In M. tuberculosis, the atp operon is downregulated during growth in macrophages (19), the mouse lung and in cells exposed to NO or hypoxia (18).”

What the sources say

• Supported

  The Expression Profiling of Intraphagosomal MTB section identifies the ATP-synthase genes in cluster III as a putative operon of repressed genes. This supports the macrophage-growth portion attributed to this paper; the mouse-lung, NO, and hypoxia portion is attached to a different citation. (LLM, conf=0.91)

  cites [19] source
• Partly supported

  The Results and Discussion report decreased atpA and atpD expression during chronic mouse-lung infection. The section on in vitro respiratory flexibility reports that both transcripts decreased under oxygen depletion, but its discussion of NO-treated cells does not establish downregulation of the atp genes. The macrophage portion is cited to a different source (19), not this paper (18). (LLM, conf=0.84)

  cites [18] sourceExperimental — accuracy not yet measured

In the paper

“These data suggest that Hyd2 oxidizes hydrogen at very low concentrations, which fits with its purported role as a high-affinity hydrogenase (52).”

What the sources say

• Partly supported

  The Results (p. 3) identify a putative high-affinity [NiFe]-hydrogenase in S. avermitilis, and the Discussion (p. 6) describes high-affinity H₂ oxidation in Streptomyces isolates possessing the relevant genes. These passages support the proposed role of that hydrogenase group, but the paper does not identify Hyd2 or establish that Hyd2 itself oxidizes H₂ at very low concentrations. (LLM, conf=0.78)

  cites [52] sourceExperimental — accuracy not yet measured

In the paper

“For example, in E. coli, cytochrome bo (Km for oxygen in the micromolar range) and cytochrome bd (Km for oxygen in the nanomolar range) (63, 64) are coordinately regulated by the ArcBA system and transcriptional regulator FNR (65).”

What the sources say

• ?Not checked — no full text of the sourcecites [63] source
• ?Not checked — no full text of the sourcecites [64] source
• Partly supported

  The Abstract and Introduction (page not available) state that ArcA/ArcB and Fnr regulate the cytochrome bd (cydAB) operon. The paper contrasts cytochrome bo and bd expression as oxygen becomes limiting, but its substantive passages do not establish that both oxidases are coordinately regulated by both regulators. The oxygen-Km values are attached to other citations in the citing sentence, not to this paper. (LLM, conf=0.79)

  cites [65] sourceExperimental — accuracy not yet measured

In the paper

“M. smegmatis lacks an MDH homologue and it was shown that MQO responded to low oxygen concentration with 4-fold increase in gene expression (16).”

What the sources say

• Supported

  The Results section (“TCA and Glyoxylate Shunt Pathways”; page not provided) states that M. smegmatis lacks NAD+-dependent malate dehydrogenase and that MQO was upregulated fourfold under hypoxia, compared with growth at 50% oxygen saturation. (LLM, conf=0.95)

  cites [16] source

In the paper

“When slow growing cells of M. smegmatis (70 h doubling time), with low levels of atp operon expression, are exposed to hypoxia (0.6% oxygen saturation), the atp operon is upregulated 3-fold suggesting an important role for this enzyme during adaptation to hypoxia (16).”

What the sources say

• Partly supported

  The Results (Energy Metabolism; page not available) report that the F1Fo-ATP synthase gene cluster was downregulated during slow growth at 50% oxygen saturation, supporting the claim of low expression. The paper also studies slow-growing cells at 0.6% oxygen saturation, but its account of the hypoxic response does not report threefold upregulation of the atp operon or assign that operon an important role in hypoxia adaptation; it instead highlights oxidases and hydrogenases. (LLM, conf=0.84)

  cites [16] sourceExperimental — accuracy not yet measured

In the paper

“Induction of EHR was independent of DosR, suggesting that other sensory and regulatory mechanisms must exist to signal prolonged exposure to hypoxia.”

What the sources say

• Supported

  The Results section ('The EHR and the DosR regulon'; page unavailable) reports that nearly all later-induced genes were also induced in the dosR mutant. The Discussion (page unavailable) likewise says disrupting the DosR regulon had very little effect on EHR expression and describes regulatory factors within the EHR. The proposed involvement of other mechanisms is consistent with those findings, though the paper does not identify a specific sensor for prolonged hypoxia. (LLM, conf=0.88)

  cites [125] sourceExperimental — accuracy not yet measured

In the paper

“In contrast, a set of 230 genes was significantly up-regulated at four and seven days of hypoxia, but not initially, and were termed the enduring hypoxic response (EHR) (125).”

What the sources say

• Supported

  The Results section, “The Enduring Hypoxic Response (EHR),” defines the EHR as MTB genes not induced initially but significantly upregulated at four and seven days of hypoxia. It states that 230 genes meet those criteria. (LLM, conf=0.95)

  cites [125] source

In the paper

“However, the fourth putative hydrogenase is only found in pathogenic mycobacteria (including M. tuberculosis complex) and seems to be restricted to slow-growers (Table 1).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites Table 1

In the paper

“Interestingly, a proC mutant of M. tuberculosis was avirulent in immunocompetent mice, however this was not due to its inability to proliferate intracellulary because bacterial loads increased in the mouse lungs after 20 days post infection (49).”

What the sources say

• ?Not checked — no full text of the sourcecites [49] source

In the paper

“The addition of TMC207, a specific inhibitor of the F1FO-ATP synthase, was bactericidal against hypoxic, non-replicating M. tuberculosis, but had no effect on the ΔΨ (6).”

What the sources say

• ?Not checked — no full text of the sourcecites [6] source

In the paper

“Early studies on respiration demonstrated that Mycobacterium tuberculosis H37Rv, grown in the lungs of infected mice, had high rates of endogenous respiration that were not stimulated by exogenous substrates (e.g. acetate, pyruvate, glucose, glycerol, lactate) (1). In contrast, cells grown in vitro respired these substrates at high rates.”

What the sources say

• ?Not checked — no full text of the sourcecites [1] source

In the paper

“Mutations in the ndh gene of M. smegmatis result in a pleitropic effect: temperature sensitivity, amino acid auxotrophy and resistance to the first-line anti-TB drug isoniazid (INH) and its analog and second-line anti-TB drug ethionamide (ETH) (14, 15).”

What the sources say

• ?Not checked — no full text of the sourcecites [14] source
• ?Not checked — no full text of the sourcecites [15] source

In the paper

“Measured experimental values for mycobacteria oxidizing NADH or succinate yield P/O ratios of 0.52, and 0.36, respectively (5).”

What the sources say

• ?Not checked — no full text of the sourcecites [5]

In the paper

“Rao et al. (6) have reported that hypoxic, non-replicating M. tuberculosis generate a total PMF of −113 mV, −73 mV of electrical potential (ΔΨ) and −41 mV of ZΔpH.”

What the sources say

• ?Not checked — no full text of the sourcecites [6] source

In the paper

“only two terminal respiratory oxidases present in mycobacteria, an aa3-type cytochrome c oxidase (encoded by ctaBCDE) belonging to the heme-copper respiratory oxidase family and cytochrome bd-type menaquinol oxidase (cydABCD) (Figure 1).”

In the paper

“Growth of mycobacteria is sensitive to compounds that dissipate the membrane potential (e.g. protonophores and valinomycin) and these compounds are bactericidal towards growing and non-growing (aerobic or hypoxic) cells”

What the sources say

• ?Not checked — no full text of the sourcecites [4] source
• ?Not checked — no full text of the sourcecites [6] source

In the paper

“The addition of thioridazine, a compound that targets NDH−2, results in dissipation of the ΔΨ and significant cell death suggesting that NADH is an important electron donor for the generation of the ΔΨ under hypoxic conditions.”

What the sources say

• ?Not checked — no full text of the sourcecites [6] source

In the paper

“Proline can be utilized as an electron donor as well as a carbon and nitrogen source (Figure 2).”

In the paper

“The PMF-generating machinery in mycobacteria comprises three energy-conserving steps: complex I (4H+/2e−), complex III (menaquinol-cytochrome c oxidoreductase, 4H+/2e−) and complex IV (2H+/2e−) suggesting that the overall proton translocation stoichiometry for the transfer of 2e− from NADH to oxygen is 10H+/2e−.”

In the paper

“Irrespective of the oxygen concentration or the protonmotive force (PMF), ATP synthesis is obligatorily coupled to the electron transport chain and the F1Fo-ATP synthase”

In the paper

“Fatty acids, however, stimulated the respiration of in vivo grown M. tuberculosis, suggesting for the first time that M. tuberculosis switches to different energy sources in host tissues to fuel respiration.”

What the sources say

• ?Not checked — no full text of the sourcecites [1] source

In the paper

“This indicates that SDH1 could be the dedicated succinate dehydrogenase and SDH2 catalyses fumarate reductase activity, which is important for survival under hypoxia.”

In the paper

“NDH-1 is encoded by the nuoABCDEFGHIJKLMN operon and transfers electrons to menaquinone, conserving energy by translocating protons across the membrane to generate a PMF (Figure 2).”

In the paper

“As an exception among mycobacteria, M. tuberculosis encodes a third complex (frdABCD) that is annotated as a fumarate reductase (Table 1) and is absent in all other pathogenic strains like Mycobacterium avium paratuberculosis, Mycobacterium marinum, Mycobacterium ulcerans and M. leprae.”

In the paper

“Succinate dehydrogenase forms complex II of the respiratory chain and couples oxidative phosphorylation to central carbon metabolism by being an integral part of the TCA cycle (Figure 2).”

In the paper

“In bacteria three different types of respiratory NADH dehydrogenases have been identified and characterized on the basis of reaction mechanism, subunit composition and protein architecture (11). These include the proton-pumping type I NADH dehydrogenase (NDH-1, complex I), non-proton pumping type II NADH dehydrogenase (NDH-2) and sodium-pumping NADH dehydrogenase (NQR).”

What the sources say

• ?Not checked — no full text of the sourcecites [11] source

In the paper

“Mycobacteria generally grow at neutral pH and under these conditions generate a PMF of approximately −180 mV (4).”

What the sources say

• ?Not checked — no full text of the sourcecites [4] source

In the paper

“In the absence of oxygen, mycobacterial growth is inhibited, even if alternative electron acceptors are present (e.g. nitrate, fumarate).”

In the paper

“In fact, it has been proposed that fumarate may be an important endogenous electron acceptor for energy production and maintenance of redox balance (oxidation of NADH to NAD+) in hypoxic non-replicating mycobacteria (6).”

What the sources say

• ?Not checked — no full text of the sourcecites [6] source

In the paper

“Hydrogenases catalyze the reversible oxidation of molecular hydrogen: 2H+ + 2e−→ H2 and play a central role in energy metabolism of bacteria, archaea and eukarya (50).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [50]

In the paper

“These results suggest that SDH2 has a pivotal role in the transition of M. tuberculosis from aerobic to hypoxic conditions and supports the hypothesis of it being a fumarate reductase.”

In the paper

“The cytochrome bd branch is bioenergetically less efficient (non-proton translocating) and is synthesized at low oxygen tensions in mycobacteria (67).”

What the sources say

• ?Not checked — no full text of the sourcecites [67] source

In the paper

“Ehr enzymes lack the cysteine residues needed to ligate a [NiFe] center, which is the catalytic center of hydrogenases. Additionally, no maturation factors to synthesize these complex centers are present in M. tuberculosis.”

In the paper

“It has been shown that M. tuberculosis H37Ra, which possesses CO-DH activity, can grow on CO as a sole source of carbon and fuel for energy generation (56) (Figure 2).”

What the sources say

• ?Not checked — no full text of the sourcecites [56] source

In the paper

“The M. tuberculosis narK2 was shown to complement this E. coli double mutant, supporting a role for narK2 in nitrate reduction by coding for a transporter of nitrate into and nitrite out of the cell (85).”

What the sources say

• ?Not checked — no full text of the sourcecites [85] source

In the paper

“This strategy does not appear to be exploited by M. smegmatis: the F1Fo-ATP synthase is essential for growth even on fermentable substrates, suggesting that ATP production from substrate level phosphorylation alone, despite increased glycolytic flux, may be insufficient to sustain growth of these bacteria (103).”

What the sources say

• ?Not checked — no full text of the sourcecites [103] source

In the paper

“These data support the proposal that nitrite produced by nitrate reductase is not converted to ammonium, but instead is exported from the cell by NarK2.”

In the paper

“Carbon monoxide dehydrogenase (CO-DH) is responsible for the oxidation of CO to carbon dioxide (CO2) in carboxydobacteria, which grow on CO as a sole source of carbon and energy (55).”

What the sources say

• ?Not checked — no full text of the sourcecites [55] source

In the paper

“Sohaskey and Wayne demonstrate that overexpression of recombinant M. tuberculosis nitrate reductase in either M. tuberculosis or M. smegmatis (low nitrate reductase activity) does not confer the ability of these cells to grow anaerobically i.e. no growth of either species is observed with nitrate anaerobically even though the nitrate reductase activity of whole cells increases (85).”

What the sources say

• ?Not checked — no full text of the sourcecites [85] source

In the paper

“The evolution of H2 is a mechanism commonly employed by anaerobic bacteria to recycle reducing equivalents obtained from anaerobic degradation of organic substrates.”

In the paper

“The M. smegmatis cydA mutant showed a reduced growth rate at 0.5–1 % air saturation and also a 10-fold difference in CFU after 140 h of growth in the presence of cyanide at 21% air saturation when co-cultured with wild-type M. smegmatis (67).”

What the sources say

• ?Not checked — no full text of the sourcecites [67] source

In the paper

“No function has yet been proposed for Ehr enzymes, but its homology to hydrogenases and to proton-pumping type I NADH dehydrogenases points to a role in energy metabolism.”

In the paper

“M. tuberculosis harbors a copy of MQO and a cytoplasmic NAD+-dependent malate dehydrogenase (MDH) (61, 62).”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [61]
• ?Not checked — no full text of the sourcecites [62] source

In the paper

“Based on these observations, it is apparent that this enzyme does not support anaerobic growth of mycobacteria and therefore the role of this enzyme in the physiology of mycobacteria is unclear.”

In the paper

“Singh and colleagues report that WhiB3 contains a 4Fe-4S cluster, which binds NO (121).”

What the sources say

• ?Not checked — no full text of the sourcecites [121] source

In the paper

“It is proposed that NarK2 senses the redox state of the cell, possibly by monitoring the flow of electrons to cytochrome oxidase, and adjusts its activity so that nitrate is transported under reducing, but not under oxidizing conditions (86).”

What the sources say

• ?Not checked — no full text of the sourcecites [86] source

In the paper

“In the absence of oxygen, alternative electron acceptors (e.g. nitrate and fumarate) are available for mycobacterial metabolism, but none of these electron acceptors have been shown to support growth of mycobacterial species.”

In the paper

“During aerobic respiration, energy is conserved by the generation of a PMF across a proton-impermeable membrane.”

In the paper

“A striking observation is that neither Dos nor WhiB3 controls any component of the electron transport machinery in M. tuberculosis.”