| Pathway ID | Pathway Name | Chemical Compounds | Proteins | Pathway Description |
---|
PW480925 | YvfT operon | Reaction compounds not found | | YvfT/YvfU controls the expression of the yvfRS operon that codes for an ABC transporter. The YvfT effector pathway is part of a two-component signal transduction system that enables bacterial cells to sense and respond to environmental stimuli. This system is governed by the YvfU regulog, in which YvfU acts as the response regulator, and YvfT functions as the sensor histidine kinase.
In this pathway:
YvfT – A sensor histidine kinase located in the cell membrane, YvfT detects specific extracellular signals (likely related to stress, nutrient availability, or other environmental conditions). Upon signal detection, YvfT undergoes autophosphorylation at a conserved histidine residue.
YvfU – A response regulator that receives the phosphate group from phosphorylated YvfT. Once activated, YvfU binds DNA to regulate the transcription of target genes in the pathway.
yvfR – Encodes a putative membrane-associated protein that may play a role in signal transduction or cellular response.
yvfS – Encodes a protein of unknown function, possibly involved in the same regulatory network or contributing to the downstream response.
BLi04302 – A gene with currently uncharacterized function, but often found in operonic association with the yvf cluster, suggesting it may contribute to the physiological response triggered by the YvfT/YvfU system. | PW543433 | Biofilm formation: epsA, epsB, epsC, epsD, epsE, epsF, epsG, epsH, epsI, epsJ, epsK, epsL, epsM, epsN, epsO operon | Reaction compounds not found | | The regulation of the epsABCDEFGHIJKLMNO operon. The operon is inhibited by sinR (HTH-type transcriptional regulator) and activated by sinI. SinR binds to the promoter inhibiting crp from binding and transcribing the operon. SinI is regulated by spo0A (Stage 0 sporulation protein A). When spo0A is present in high concentrations, sinI is expressed. Then sinI binds with sinR to form a sinI-sinR heterodimer. This caused conformational changes to sinR preventing it from binding the to promoter. Therefore, activating the expression of the operon. There are 15 products from this operon: epsA (Polysaccharide chain length determinant N-terminal domain-containing protein), epsB (non-specific protein-tyrosine kinase), epsC (Probable polysaccharide biosynthesis protein), epsD (Putative glycosyltransferase), epsE (Putative glycosyltransferase), epsF (Putative glycosyltransferase), epsG (Transmembrane protein), epsH (Putative glycosyltransferase), epsI (Putative pyruvyl transferase), epsJ (Uncharacterized glycosyltransferase), epsK (Uncharacterized membrane protein EpsK), epsL (Uncharacterized sugar transferase), epsM (UDP-N-acetylbacillosamine N-acetyltransferase), epsN (Putative pyridoxal phosphate-dependent aminotransferase), epsO (Putative pyruvyl transferase). EpsA, epsC, epsG, epsK, epsL are membrane proteins involved in biofilm formation. EpsD, epsE, epsF, epsH, epsI, epsJ, epsN and epsO are types of transferases used in the EPS production. EpsB is an enzyme used to phosphorylate tyrosine residue proteins. EpsM is an enzyme used to add an acetyl group to UDP-N-acetylbacillosamine to make UDP-N,N'-diacetylbacillosamine. | PW543653 | Copper ion, (Cu+) - CsoR operon | Reaction compounds not found | | Copper efflux regulator CsoR is involved in the regulation of ycnJ expression, leading to a new model for copper homeostasis in B. subtilis. CsoR from Bacillus subtilis, which is encoded upstream of the copZA operon, is 37% homologous to M. tuberculosis CsoR, and elevated copper levels in B. subtilis are sensed by CsoR, which leads to derepression of the copZA copper efflux operon. Under low intracellular Cu? conditions, CsoR binds to promoter regions of copper efflux genes and represses their transcription. When Cu? levels rise, Cu? binds directly to CsoR, causing it to release from DNA, thereby derepressing genes involved in copper efflux and sequestration.
The copper ion (Cu?) effector pathway is a bacterial homeostasis and detoxification system that protects cells from the toxic effects of excess monovalent copper (Cu?) while ensuring its availability for essential enzymatic functions. This pathway is regulated by CsoR (Copper-sensitive operon Repressor), a Cu?-responsive transcriptional regulator.
Key components of the CsoR regulog include:
csoR – Encodes the CsoR transcriptional repressor itself, forming part of a feedback loop that maintains copper homeostasis by sensing and responding to intracellular Cu? concentrations.
copA – Encodes a P-type ATPase copper efflux pump, which actively exports excess Cu? from the cytoplasm to prevent toxicity.
copZ – Encodes a copper chaperone protein that binds and safely delivers Cu? to target proteins or to CopA for efflux, preventing uncontrolled copper-mediated redox reactions and oxidative damage. | PW554279 | Biofilm formation: tapA, sipW, tasA operon | Reaction compounds not found | | The regulation of the tapA, sipW, tasA operon. The operon is inhibited by sinR (HTH-type transcriptional regulator) and activated by sinI. SinR binds to the promoter inhibiting crp from binding and transcribing the operon. SinI is regulated by spo0A (Stage 0 sporulation protein A). When spo0A is present in high concentrations, sinI is expressed. Then sinI binds with sinR to form a sinI-sinR heterodimer. This caused conformational changes to sinR preventing it from binding the to promoter. Therefore, activating the expression of the operon. The products of this operon are: tapA (TasA anchoring/assembly protein), sipW (Signal peptidase I W) and tasA (Major biofilm matrix component). TasA and tapA are transported out of the cell and form a major component of the biofilm. TasA forms fibers important for the structure of the biofilm and tapA anchors the tasA fibers to the cell membrane. | PW571133 | Glycine betaine synthesis: gbsA, gbsB operon | Reaction compounds not found | | The regulation of the gbsAB operon. The operon is inhibited by gbsR (HTH-type transcriptional repressor) and activated by high concentrations of choline. GbsR binds to the promoter preventing crp from binding and transcribing the operon. Choline is transported into the cell by the opuBB (Choline transport system permease protein) and opuC (opuCC, opuCD, opuCB, opuCA) transporters. Both of these transporters used ATP to bring in choline. When choline is in high concentration, it binds with gbsR causing conformational changes. These conformational changes prevent gbsR from binding to the promoter, allowing crp to transcribe the operon. The products of this operon are two enzymes: gbsA (Betaine aldehyde dehydrogenase) and gbsB (Choline dehydrogenase). Both enzymes are used in the two step process of breaking down choline to betaine. GbsB is used to break down choline to betaine aldehyde. GbsA is used to break down betaine aldehyde to betaine. | PW571148 | Proline utilization: putB, putC, putP operon | Reaction compounds not found | | The regulation of the putBCP operon. The operon is activated by both the presence of proline and putR (Proline-responsive transcriptional activator). Therefore, the operon is inhibited by the absence of proline. The operon can also be inhibited by high concentration of proline due to the cell protecting itself from high osmolarity. Proline is brought into the cell by the putP (High-affinity proline transporter) and opuE (Osmoregulated proline transporter) transporters. When proline is present in the cell, putR binds to the promoter which is essential for the transcription of the operon. When proline is absent or in high concentration, putR releases the promoter inhibiting the transcription of the operon. There are three products of this operon: putB (Proline dehydrogenase 2), putC (1-pyrroline-5-carboxylate dehydrogenase 2) and putP. PutP is a transporter used in proline transportation into the cell. PutB and putC are enzymes used to turn proline into glutamate. PutB turns proline into 1-pyrroline-5-carboxylate. 1-pyrroline-5-carboxylate spontaneously changes to L-glutamate 5-semialdehyde with the addition of water. The reverse also occurs spontaneously with the removal of water. PutC turns L-glutamate 5-semialdehyde to glutamate. | PW583876 | Copper ion, (Cu+) - YcnK operon | Reaction compounds not found | | The copper ion (Cu?) effector pathway regulated by the YcnK regulog is involved in copper acquisition and homeostasis in bacterial cells, particularly under conditions of copper limitation. While copper is an essential micronutrient required for the activity of many enzymes, its uptake must be tightly controlled due to its redox reactivity and potential toxicity.
YcnK is a transcriptional activator of the GntR family that senses intracellular copper status and regulates the expression of genes involved in copper uptake. Under low copper conditions, YcnK activates transcription of its target genes to promote copper acquisition.
Key genes in the YcnK regulog include:
ycnK – Encodes the YcnK transcriptional regulator itself, which controls its own expression and that of downstream genes in response to copper availability.
ycnJ – Encodes a putative copper importer, likely functioning as a membrane protein that facilitates high-affinity uptake of Cu? into the cell under copper-limiting conditions.
ycnI – Encodes a conserved DUF1775 domain-containing protein, possibly involved in copper binding, sensing, or delivery to cuproenzymes, though its exact function remains under investigation. | PW583895 | Catechin operon | Reaction compounds not found | | Bacillus subtilis LmrA is known to be a repressor that regulates the lmrAB and yxaGH operons; lmrB and yxaG encode a multidrug resistance pump and quercetin 2,3-dioxygenase, respectively. The catechin effector pathway is part of a bacterial response system that enables detoxification or resistance to catechins, a group of plant-derived polyphenolic compounds with antimicrobial properties. This pathway is regulated by the LmrA regulog, in which LmrA acts as a transcriptional regulator that responds to the presence of catechins or related stress-inducing compounds.
LmrA typically regulates genes that help counteract the oxidative or membrane-disrupting effects of catechins, supporting bacterial survival in plant-associated or polyphenol-rich environments.
Key genes in the LmrA regulog include:
yxaG – Encodes a glutathione-dependent epoxide hydrolase, an enzyme potentially involved in detoxifying reactive epoxide intermediates generated by catechin metabolism or stress responses.
qodI – Encodes a quinone oxidoreductase, which likely contributes to redox balancing by reducing quinones and mitigating oxidative stress triggered by catechins. | PW598206 | Neotrehalosadiamine biosynthesis: ntdA, ntdB, ntdC operon | Reaction compounds not found | | The regulation of the ntdABC operon. The operon is activated by ntdR (NTD biosynthesis operon regulator) and neotrehalosadiamine. The operon is inhibited by glcP (Glucose/mannose transporter). NtdR is required for the proper function of crp in transcription of the operon and ntdR cannot bind to the promoter without neotrehalosadiamine. GlcP controls the amount of glucose that is present inside the cell (acts as a glucose sensor), therefore, it indirectly inhibits ntdR function. There are three products from this operon: ntdA (3-oxo-glucose-6-phosphate:glutamate aminotransferase), ntdB (Kanosamine-6-phosphate phosphatase) and ntdC (Glucose-6-phosphate 3-dehydrogenase). These products are all enzymes used in the biosynthesis of neotrehalosadiamine from glucose. NtdC is used to turn D-glucose-6-phosphate (imported into the cell by ptsG: PTS system glucose-specific EIICBA component) to 3-dehydro-D-glucose-6-phosphate. NtdA is used to turn 3-dehydro-D-glucose-6-phosphate to D-kanosamine-6-phosphate. NtdB is used to turn D-kanosamine-6-phosphate to kanosamine. The process of kanosamine to neotrehalosadiamine is unknown. | PW598226 | Ramoplanin resistance: ytrA, ytrB, ytrC, ytrD, ytrE, ytrF operon | Reaction compounds not found | | The regulation of ytrABCDEF Operon. The operon is inhibited by ytrA (HTH-type transcriptional repressor) and activated indirectly by Ramoplanin. Ramoplanin indirectly inhibits ytrA by altering or damaging the peptidoglycan production. When there is peptidoglycan disruption, ytrA releases the promoter allowing crp to transcribe the operon. The operon has 6 products: ytrA, ytrB (ABC transporter ATP-binding protein), ytrC (Probable ABC transporter permease), ytrD (Probable ABC transporter permease), ytrE (ABC transporter ATP-binding protein) and ytrF (ABC transporter permease). All the products (not ytrA) form a transporter which is important for acetoin utilization. | PW598229 | Inositol utilization: iolR, iolS operon | Reaction compounds not found | | The regulation of the iolRS operon. The operon is inhibited by iolR (HTH-type transcriptional regulator) and activated by the presence of inositol. Glucose can also contribute to the inhibition of the operon. The operon has two products: iolR and iolS (Aldo-keto reductase). The function of iolS is unknown. | PW598247 | Galactan utilization: ganS, ganP, ganQ, ganA, ganB operon | Reaction compounds not found | | The regulation of the ganSPQAB operon. The operon is inhibited by ganR (HTH-type transcriptional regulator) and glucose. The operon in activated by the presence of galactobiose which is transported into the cell by the ganSPQ transporter. GanR bind to the promoter, inhibiting the expression of the operon. When galactobiose is present, it binds to ganR causing it to release the promoter. The operon has five products: ganS (Galactooligosaccharide-binding protein), ganP (Galactooligosaccharides transport system permease protein), ganQ (Galactooligosaccharides transport system permease protein), ganA (Beta-galactosidase) and ganB (O07013). GanS, ganP, ganQ and msmX (Oligosaccharides import ATP-binding protein) form an ABC transporter involved in the transport of galactobiose into the cell. The other two products are enzymes used in the utilization of galactan (galactan to galactose). GanB is used to turn galactan to galactobiose in the extracellular space (the enzyme is secreted out of the cell). GanA is used to turn galactobiose to galactose inside the cell. | PW611334 | Sulfate operon | Reaction compounds not found | | The sulfate effector pathway is a bacterial system dedicated to the assimilation of inorganic sulfate (SO?²?) and its conversion into reduced sulfur compounds needed for the biosynthesis of essential sulfur-containing amino acids (e.g., cysteine and methionine) and cofactors. This pathway is tightly regulated by CysL, a LysR-type transcriptional regulator that responds to intracellular sulfur levels.
Under sulfur-limiting conditions, CysL activates the expression of genes involved in sulfate uptake, activation, and reduction. This ensures efficient assimilation of sulfate when reduced sulfur compounds are scarce in the environment.
Key genes in the CysL regulog include:
Sulfate activation and reduction:
sat – Encodes sulfate adenylyltransferase, which activates sulfate by converting it into adenosine 5?-phosphosulfate (APS).
cysC – Encodes APS kinase, which phosphorylates APS to form 3?-phosphoadenosine 5?-phosphosulfate (PAPS), an intermediate in both assimilatory and dissimilatory sulfate reduction.
cysH – Encodes PAPS reductase, which reduces PAPS to sulfite (SO?²?), a key step in the assimilatory sulfate reduction pathway.
cysJ and cysI – Encode the two subunits of sulfite reductase, which catalyze the final step of sulfate assimilation by reducing sulfite to sulfide (S²?), which can then be incorporated into cysteine.
Accessory and regulatory proteins:
ylnD, sirB, sirC – Likely encode accessory proteins or alternative components of the sulfite reductase complex or regulatory factors that enhance the efficiency and regulation of sulfate reduction.
yjjA – Putative redox or sulfur metabolism-related gene that may contribute to maintaining the cellular redox environment during sulfur assimilation.
BH3384 – A gene of unknown function, often co-regulated with sulfate reduction genes, potentially playing a supportive role in sulfur metabolism or stress response. | PW611361 | 5-phosphoribosyl 1-pyrophosphate operon | Reaction compounds not found | | The 5-phosphoribosyl 1-pyrophosphate (PRPP) effector pathway is a central metabolic route responsible for the de novo biosynthesis of purine nucleotides (AMP and GMP), which are essential for DNA, RNA, energy metabolism, and cellular signaling. This pathway is tightly regulated by PurR, a purine-responsive transcriptional repressor.
PurR senses intracellular purine levels and represses the expression of purine biosynthesis genes when purines are abundant. When purine levels are low, PurR repression is relieved, allowing the transcription of genes necessary for building purines from basic metabolic precursors, with PRPP as the starting substrate.
In response to a signal of excess adenine, represses the transcription of the pur operon, which encodes enzymes of the purine biosynthetic pathway.
Key genes in the PurR regulog include:
Core de novo purine biosynthesis genes:
purF – Encodes amidophosphoribosyltransferase, catalyzing the first committed step of the pathway: the conversion of PRPP to phosphoribosylamine.
purD – Encodes GAR synthetase, catalyzing the formation of glycinamide ribonucleotide (GAR).
purN – Encodes GAR transformylase, which converts GAR to formyl-GAR.
purL, purQ, purS – These form a multi-subunit enzyme complex (FGAM synthetase) that converts formyl-GAR to formylglycinamidine ribonucleotide (FGAM).
purM – Encodes AIR synthetase, catalyzing the formation of aminoimidazole ribonucleotide (AIR).
purE – Encodes N5-CAIR mutase, converting AIR into carboxyaminoimidazole ribonucleotide (CAIR).
purK – Encodes N5-CAIR synthetase, functioning upstream of purE in CAIR formation.
purC – Encodes SAICAR synthetase, catalyzing the conversion of CAIR to SAICAR.
purB – Encodes adenylosuccinate lyase, which participates in two reactions: conversion of SAICAR to AICAR and of adenylosuccinate to AMP.
purH – Encodes a bifunctional enzyme with AICAR transformylase and IMP cyclohydrolase activities, catalyzing the final steps in IMP (inosine monophosphate) synthesis.
Downstream conversion of IMP:
purA – Encodes adenylosuccinate synthetase, converting IMP to AMP.
guaC – Encodes GMP reductase, contributing to purine interconversion and balance between AMP and GMP pools.
Accessory genes:
fhs – Encodes formyltetrahydrofolate synthetase, which generates the one-carbon donor (10-formyl-THF) required for GAR and AICAR formylation steps.
LGG_02640 – Likely encodes a gene co-expressed with purine biosynthetic genes, possibly involved in folate metabolism or regulation. |
|
---|