FliA (sigma-28, sigma^F) is an alternative sigma factor belonging to the sigma-70 family that directs RNA polymerase to flagellar gene promoters in D. vulgaris Hildenborough. As the master regulator of late flagellar gene expression (class III/IV genes), FliA controls transcription of genes encoding flagellin (fliC), hook-associated proteins, motor components (motAB), and chemotaxis machinery. FliA activity is regulated by the anti-sigma factor FlgM, which sequesters FliA in the cytoplasm until hook-basal body (HBB) assembly is complete; upon HBB completion, FlgM is secreted through the flagellar type III export apparatus, releasing FliA to drive late gene expression. Deletion of fliA in D. vulgaris results in severe motility defects, defective/truncated flagella, and loss of biofilm formation capacity.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:2000142 regulation of DNA-templated transcription initiation | IEA GO_REF:0000108 | ACCEPT | Summary: FliA (sigma-28) regulates transcription initiation by directing RNA polymerase to sigma-28-dependent promoters of late flagellar genes. The annotation to "regulation of DNA-templated transcription initiation" is accurate since sigma factors specifically function in transcription initiation rather than elongation. However, this term is generic and does not capture the flagellar-specific function. Reason: This annotation correctly reflects that FliA functions in regulation of transcription initiation. Sigma factors are initiation factors that promote attachment of RNA polymerase to specific promoter sequences and are released after initiation (UniProt Q726C4). While a more specific term involving flagellar regulation would be ideal, no such term exists in GO. The IEA annotation via logical inference (GO_REF:0000108) is appropriate. Supporting Evidence: file:DESVH/Q726C4/Q726C4-deep-research-falcon.md FliA is an alternative sigma factor that associates with RNA polymerase core in the cytosol to initiate transcription from sigma-28 promoters |
| GO:0003677 DNA binding | IEA GO_REF:0000120 | ACCEPT | Summary: FliA/sigma-28 contains conserved sigma-70 regions 2 and 4 that mediate DNA element recognition at promoters. While sigma factors do not bind DNA autonomously, they confer DNA-binding specificity when combined with RNA polymerase core to form the holoenzyme. The annotation is technically correct but somewhat imprecise. Reason: The DNA binding annotation is acceptable because sigma factors confer DNA-binding specificity to the RNAP holoenzyme by recognizing specific promoter elements. FliA contains the characteristic sigma-70 region 2 and region 4 domains (IPR007627, IPR007630) that recognize the -10 and -35 promoter elements respectively. The sigma-28 promoter consensus is approximately TAAA-N15-GCCGATAA. Supporting Evidence: file:DESVH/Q726C4/Q726C4-deep-research-falcon.md FliA contains conserved sigma-70 regions that mediate promoter recognition and RNA polymerase core binding, with regions 2 and 4 central to DNA element recognition |
| GO:0003700 DNA-binding transcription factor activity | IEA GO_REF:0000120 | MODIFY | Summary: This annotation characterizes FliA as a DNA-binding transcription factor. While sigma factors do regulate transcription and confer promoter specificity, the term "DNA-binding transcription factor activity" is typically used for sequence-specific DNA-binding proteins that directly bind DNA and regulate transcription of target genes. Sigma factors function differently - they bind RNA polymerase core and confer promoter specificity to the holoenzyme. Reason: The term "DNA-binding transcription factor activity" (GO:0003700) is not the most precise term for sigma factors. GO:0016987 (sigma factor activity) is the more appropriate molecular function term that specifically describes the mechanism by which sigma factors promote transcription initiation. This annotation should be replaced with the more specific sigma factor activity term. Proposed replacements: sigma factor activity |
| GO:0003899 DNA-directed RNA polymerase activity | IEA GO_REF:0000002 | REMOVE | Summary: This annotation incorrectly attributes RNA polymerase catalytic activity to FliA. Sigma factors do not possess RNA polymerase enzymatic activity themselves; rather, they are regulatory subunits that associate with the RNA polymerase core enzyme (alpha2-beta-beta') to direct promoter recognition. The catalytic activity resides in the core enzyme subunits, not the sigma factor. Reason: FliA is a sigma factor, not an RNA polymerase enzyme. Sigma factors function by binding to the RNA polymerase core to form a holoenzyme and directing it to specific promoters; they do not possess catalytic polymerase activity. This annotation appears to be an over-annotation based on InterPro domain associations (GO_REF:0000002). The UniProt record correctly identifies Q726C4 as "RNA polymerase sigma factor" not as RNA polymerase itself. This distinction is critical for accurate functional annotation. Supporting Evidence: file:DESVH/Q726C4/Q726C4-deep-research-falcon.md FliA is an alternative sigma factor that associates with RNA polymerase core in the cytosol to initiate transcription from sigma-28 promoters |
| GO:0006352 DNA-templated transcription initiation | IEA GO_REF:0000002 | ACCEPT | Summary: FliA is directly involved in DNA-templated transcription initiation as it binds RNA polymerase core and directs the holoenzyme to sigma-28-dependent promoters of late flagellar genes. Upon promoter recognition and initiation, sigma factors are released from the elongating polymerase. Reason: This biological process annotation is accurate. Sigma factors function specifically in transcription initiation - they bind RNAP core to form the holoenzyme, recognize and bind promoter sequences, facilitate open complex formation, and are released after initiation. FliA participates in transcription initiation of late flagellar genes including flagellin, hook-associated proteins, motor components, and chemotaxis genes. Supporting Evidence: file:DESVH/Q726C4/Q726C4-deep-research-falcon.md FliA (sigma-28) directs transcription of the late (class III/IV) flagellar regulon, which typically includes flagellin (fliC), hook-associated proteins, motor components (e.g., motAB), and chemotaxis genes |
| GO:0006355 regulation of DNA-templated transcription | IEA GO_REF:0000120 | ACCEPT | Summary: FliA clearly functions in regulation of transcription as it controls expression of late flagellar genes. This annotation is accurate but somewhat general - FliA specifically regulates transcription initiation rather than elongation or other aspects of transcription. Reason: This annotation is correct. FliA regulates transcription of late flagellar genes by directing RNA polymerase to sigma-28-dependent promoters. The D. vulgaris fliA deletion mutant shows severe motility defects and defective flagella, demonstrating FliA's essential role in regulating expression of flagellar genes (Ray et al. 2014, Clark 2008). Supporting Evidence: file:DESVH/Q726C4/Q726C4-deep-research-falcon.md D. vulgaris phenotypes: delta-fliA (DVU_3229) shows (i) severe motility defects on soft agar and wet mounts; (ii) defective or truncated flagella by TEM; (iii) failure to form biofilm under tested conditions |
| GO:0016987 sigma factor activity | IEA GO_REF:0000120 | ACCEPT | Summary: This is the core molecular function annotation for FliA. Sigma factor activity precisely describes FliA's function as a promoter specificity subunit that associates with RNA polymerase core and directs it to specific promoter sequences. FliA belongs to the sigma-70 family, specifically the FliA/WhiG clade (IPR012845). Reason: This is the most accurate and informative molecular function annotation for FliA. GO:0016987 (sigma factor activity) precisely defines the mechanism by which FliA functions: it combines with RNA polymerase core to form a holoenzyme, confers promoter binding specificity, and is released after transcription initiation begins. This annotation is strongly supported by domain architecture (sigma-70 regions 2 and 4), family membership (FliA/WhiG subfamily), and functional evidence from D. vulgaris mutant studies. Supporting Evidence: file:DESVH/Q726C4/Q726C4-deep-research-falcon.md FliA is an alternative sigma factor that associates with RNA polymerase core in the cytosol to initiate transcription from sigma-28 promoters |
| GO:1902208 regulation of bacterial-type flagellum assembly | IMP PMID:24639670 Exploring the role of CheA3 in Desulfovibrio vulgaris Hilden... | NEW | Summary: FliA regulates late flagellar gene expression which is essential for flagellar assembly. Deletion of fliA in D. vulgaris results in defective or truncated flagella as shown by TEM (Ray et al. 2014). Reason: This annotation is strongly supported by organism-specific experimental evidence. The delta-fliA mutant in D. vulgaris Hildenborough shows defective or truncated flagella by transmission electron microscopy, demonstrating that FliA is required for proper flagellar assembly. FliA regulates expression of late flagellar genes (class III/IV) including flagellin and hook-associated proteins that are essential for flagellum structure. Supporting Evidence: file:DESVH/Q726C4/Q726C4-deep-research-falcon.md the D. vulgaris delta-fliA mutant (DVU3229) for FliA, predicted to regulate flagella-related genes including cheA3, was defective both in flagellum formation and in forming the motility halos PMID:24639670 Exploring the role of CheA3 in Desulfovibrio vulgaris Hildenborough motility. |
| GO:0071973 bacterial-type flagellum-dependent cell motility | IMP PMID:24639670 Exploring the role of CheA3 in Desulfovibrio vulgaris Hilden... | NEW | Summary: FliA is essential for motility in D. vulgaris. Delta-fliA mutants show severe motility defects in both soft agar assays and wet-mount microscopy (Ray et al. 2014, Clark 2008). Reason: Direct experimental evidence from D. vulgaris Hildenborough demonstrates that fliA deletion results in severe motility defects. The delta-fliA mutant (JW9017) shows loss of motility on soft agar plates and in wet-mount assays. This phenotype is consistent with FliA's role in regulating late flagellar genes required for functional flagella and cell motility. Supporting Evidence: file:DESVH/Q726C4/Q726C4-deep-research-falcon.md D. vulgaris phenotypes: delta-fliA (DVU_3229) shows (i) severe motility defects on soft agar and wet mounts; (ii) defective or truncated flagella by TEM; (iii) failure to form biofilm under tested conditions PMID:24639670 Exploring the role of CheA3 in Desulfovibrio vulgaris Hildenborough motility. |
| GO:0005737 cytoplasm | IEA file:DESVH/Q726C4/Q726C4-deep-research-falcon.md | NEW | Summary: FliA is a cytoplasmic sigma factor that associates with RNA polymerase core in the cytosol. Its activity is regulated by the anti-sigma factor FlgM, which sequesters FliA in the cytoplasm until hook-basal body assembly is complete. Reason: FliA functions in the cytoplasm where it associates with RNA polymerase core enzyme. Literature explicitly states FliA associates with RNA polymerase core in the cytosol. This localization is consistent with the function of sigma factors which must interact with cytoplasmic RNAP core to form the holoenzyme. Supporting Evidence: file:DESVH/Q726C4/Q726C4-deep-research-falcon.md FliA is an alternative sigma factor that associates with RNA polymerase core in the cytosol to initiate transcription from sigma-28 promoters |
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Download this section (compressed HTML)Q: What is the specific promoter sequence recognized by FliA in D. vulgaris? Is it similar to the consensus TAAA-N15-GCCGATAA found in other bacteria?
Q: Does D. vulgaris encode a FlgM anti-sigma factor ortholog, and if so, does it function similarly to regulate FliA activity?
Q: What is the complete FliA regulon in D. vulgaris? Which specific genes are transcribed from sigma-28-dependent promoters?
Experiment: ChIP-seq to identify FliA binding sites genome-wide in D. vulgaris and define the sigma-28 promoter consensus sequence for this organism.
Hypothesis: FliA binds to sigma-28-like promoter sequences upstream of late flagellar genes
Type: ChIP-seq
Experiment: RNA-seq comparing wild-type and delta-fliA strains to define the complete FliA regulon and identify all sigma-28-dependent genes.
Hypothesis: FliA deletion will result in downregulation of late flagellar genes
Type: RNA-seq
Experiment: Complementation studies to confirm that the motility and flagellar defects in delta-fliA are specifically due to loss of FliA function.
Hypothesis: Expression of wild-type fliA will restore motility and flagellar assembly in delta-fliA mutants
Type: Genetic complementation
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