DimA (Basic-leucine zipper transcription factor A; DIF insensitive mutant A) is a bZIP/bRLZ transcription factor of the social amoeba Dictyostelium discoideum that is required for cellular responses to the chlorinated signalling molecule DIF-1. Acting in the nucleus, DimA binds DNA as a dimer through its basic region-leucine zipper and both activates prestalk (pstO) gene expression and represses prespore gene expression downstream of DIF-1. It forms homodimers and heterodimerizes with the related bZIP factor DimB, and in response to DIF-1 it accumulates rapidly in the nucleus, a relocalization that depends on DimB. Through this transcriptional control DimA integrates DIF-1 signalling with cell-type differentiation and patterning during multicellular development, being required for stalk-cell differentiation and for repression of the spore fate; loss of dimA produces long thin slugs, cell-autonomous differentiation defects, and exclusion of mutant cells from the spore mass.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0005634 nucleus | IBA GO_REF:0000033 | ACCEPT | Summary: Nuclear localization is correct and is directly supported for DimA, which accumulates in the nucleus in response to DIF-1 where it acts as a transcription factor. Reason: As a bZIP transcription factor DimA acts in the nucleus, consistent with direct evidence of DIF-1-induced nuclear accumulation. The phylogenetic inference agrees with the experimental data for this gene product. Supporting Evidence: PMID:16410410 upon DIF-1 stimulation, DimA and DimB rapidly accumulate in the nucleus |
| GO:0010468 regulation of gene expression | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: DimA regulates the expression of prestalk and prespore genes in response to DIF-1, so regulation of gene expression is correct, though it is a broad grouping term relative to the more specific transcriptional-regulation annotations. Reason: The term is accurate but general; the more specific regulation of DNA-templated transcription (GO:0006355) better captures the core activity. Retained as a valid but non-core grouping annotation. Supporting Evidence: PMID:16410410 DimA functions as both an activator of prestalk gene expression and repressor of prespore gene expression |
| GO:0043565 sequence-specific DNA binding | IBA GO_REF:0000033 | ACCEPT | Summary: As a bZIP/bRLZ factor DimA binds DNA sequence-specifically through its basic region. This is a core molecular function. Reason: DimA is a basic-region leucine-zipper transcription factor; sequence-specific DNA binding is intrinsic to this class and is consistent with its role as a direct transcriptional regulator of DIF-1 target genes. Supporting Evidence: PMID:14729573 encodes a bZIP/bRLZ transcription factor, which is |
| GO:0003700 DNA-binding transcription factor activity | IEA GO_REF:0000002 | ACCEPT | Summary: DimA is a bZIP DNA-binding transcription factor that activates prestalk and represses prespore genes; this is a core molecular function. Reason: The InterPro bZIP-based inference matches the experimentally established role of DimA as a direct transcriptional regulator of DIF-1 responsive genes. Supporting Evidence: PMID:16410410 DimA functions as both an activator of prestalk gene expression and repressor of prespore gene expression |
| GO:0005634 nucleus | IEA GO_REF:0000044 | ACCEPT | Summary: Nuclear localization based on UniProt subcellular location mapping; correct and supported by direct evidence of DIF-1-induced nuclear accumulation. Reason: The nucleus is the site of DimA action as a transcription factor, and DimA accumulates there in response to DIF-1. Supporting Evidence: PMID:16410410 upon DIF-1 stimulation, DimA and DimB rapidly accumulate in the nucleus |
| GO:0006355 regulation of DNA-templated transcription | IEA GO_REF:0000002 | ACCEPT | Summary: DimA directly regulates transcription of DIF-1 target genes, activating prestalk and repressing prespore markers. This is a core biological process. Reason: Consistent with the experimentally established role of DimA as a direct transcriptional regulator downstream of DIF-1. Supporting Evidence: PMID:16410410 DimA functions as both an activator of prestalk gene expression and repressor of prespore gene expression |
| GO:0005634 nucleus | IDA PMID:16410410 bZIP transcription factor interactions regulate DIF response... | ACCEPT | Summary: Direct evidence that DimA:GFP accumulates in the nucleus upon DIF-1 stimulation, where it acts as a transcription factor. Core localization. Reason: GFP-fusion imaging directly demonstrated rapid, DIF-1-dependent nuclear accumulation of DimA, confirming the nucleus as its site of action. Supporting Evidence: PMID:16410410 both DimA:GFP and DimB:GFP exhibited nuclear accumulation PMID:16410410 nuclear accumulation of DimA in response to DIF-1 is dependent on DimB |
| GO:0031287 positive regulation of sorocarp stalk cell differentiation | IMP PMID:16410410 bZIP transcription factor interactions regulate DIF response... | ACCEPT | Summary: DimA is required for DIF-1-induced prestalk gene induction and stalk-cell differentiation; dimA mutant cells fail to induce prestalk markers and do not form stalk cells in response to DIF-1. Reason: DimA acts as an activator of prestalk gene expression and is required for stalk-cell differentiation, a central part of its developmental role. Supporting Evidence: PMID:16410410 DimA functions as both an activator of prestalk gene expression and repressor of prespore gene expression PMID:16410410 prestalk markers are not induced and prespore markers are not repressed |
| GO:0043944 negative regulation of asexual sporulation resulting in formation of a cellular spore | IMP PMID:16410410 bZIP transcription factor interactions regulate DIF response... | ACCEPT | Summary: DimA represses the prespore/spore fate in response to DIF-1; spore cell formation is repressed by DimA, and dimA mutants fail to repress prespore markers. Reason: Repression of prespore gene expression and spore formation is a core, experimentally established function of DimA downstream of DIF-1. Supporting Evidence: PMID:16410410 spore cell formation is repressed by DimA PMID:16410410 prestalk markers are not induced and prespore markers are not repressed |
| GO:0005737 cytoplasm | IDA PMID:16410410 bZIP transcription factor interactions regulate DIF response... | KEEP AS NON CORE | Summary: In the absence of DIF-1, DimA:GFP is fairly uniformly distributed throughout the cell (including the cytoplasm), redistributing to the nucleus upon DIF-1 stimulation. Cytoplasmic localization is thus the resting-state distribution rather than the functional site of action. Reason: The cytoplasmic localization is directly observed but represents the unstimulated distribution; the functional site of DimA is the nucleus, so this is retained as a non-core annotation. Supporting Evidence: PMID:16410410 In the absence of DIF-1, GFP was fairly uniformly distributed throughout the cells |
| GO:0005515 protein binding | IPI PMID:16410410 bZIP transcription factor interactions regulate DIF response... | KEEP AS NON CORE | Summary: This IPI annotation reflects the direct interaction between DimA and the related bZIP factor DimB, demonstrated by in vitro pull-down assays. The bare protein binding term is uninformative; the more specific dimerization activity (with DimB) captures the actual function. Reason: Protein binding (GO:0005515) is too general to convey function. The underlying DimA-DimB heterodimerization is better represented by protein dimerization activity, captured in core_functions. Retained as non-core. Supporting Evidence: PMID:16410410 DimA and DimB can form homodimeric and heterodimeric complexes in vitro |
| GO:0045595 regulation of cell differentiation | IMP PMID:14729573 A bZIP/bRLZ transcription factor required for DIF signaling ... | KEEP AS NON CORE | Summary: DimA is required to integrate DIF-1 signalling and cell-type differentiation; dimA mutants show cell-autonomous defects in cell type differentiation. This broad term is correct but subsumed by the more specific prestalk/prespore differentiation annotations. Reason: Accurate but general; the specific roles in stalk-cell differentiation and prespore repression are captured by more precise terms. Retained as a non-core grouping annotation. Supporting Evidence: PMID:14729573 the dimA(-) mutant exhibits cell autonomous |
| GO:1903013 response to differentiation-inducing factor 1 | IMP PMID:14729573 A bZIP/bRLZ transcription factor required for DIF signaling ... | ACCEPT | Summary: DimA is required for every DIF-1 response investigated; the dimA mutant produces DIF-1 but cannot respond to it. This is the defining, core function of DimA. Reason: The response to DIF-1 is the central, experimentally defined role of DimA, established by mutant phenotype and by DIF-1-induced nuclear accumulation. A core biological process. Supporting Evidence: PMID:14729573 the dimA(-) mutant produces DIF-1 but PMID:16410410 direct regulators of cellular responses to DIF-1 |
| GO:0042802 identical protein binding | IPI PMID:16410410 bZIP transcription factor interactions regulate DIF response... | ACCEPT | Summary: DimA forms homodimeric complexes in vitro, consistent with bZIP factors binding DNA as dimers. Identical protein binding (homodimerization) is a relevant molecular function. Reason: Homodimerization of DimA was directly demonstrated by pull-down assays and is functionally important, as bZIP transcription factors bind DNA as dimers. Supporting Evidence: PMID:16410410 DimA and DimB can form homodimeric and heterodimeric complexes in vitro |
| GO:0043565 sequence-specific DNA binding | IDA PMID:14729573 A bZIP/bRLZ transcription factor required for DIF signaling ... | ACCEPT | Summary: Direct-evidence annotation for sequence-specific DNA binding by the bZIP/bRLZ factor DimA. Core molecular function. Reason: DimA is a basic-region leucine-zipper DNA-binding transcription factor; sequence-specific DNA binding is intrinsic to its function as a direct regulator of DIF-1 target genes. Supporting Evidence: PMID:14729573 encodes a bZIP/bRLZ transcription factor, which is |
| GO:0012501 programmed cell death | IMP PMID:16410410 bZIP transcription factor interactions regulate DIF response... | KEEP AS NON CORE | Summary: In the 8-Br-cAMP monolayer assay DimA is proposed to trigger non-vacuolar cell death (NVCD) as the first step toward stalk-cell formation, linking DimA to a programmed cell death pathway. This is a downstream developmental consequence rather than a core molecular activity. Reason: DimA acts upstream of an NVCD/programmed cell death step during stalk-cell differentiation, but this is a peripheral developmental role of the transcription factor rather than its core function. Supporting Evidence: PMID:16410410 The first step would require DimA to trigger NVCD, whereas subsequent vacuolisation requires DimB |
| GO:0030587 sorocarp development | IMP PMID:14729573 A bZIP/bRLZ transcription factor required for DIF signaling ... | KEEP AS NON CORE | Summary: dimA mutants show hallmark developmental morphological defects (long, thin slugs and aberrant culmination) and cell-type differentiation defects, placing DimA within sorocarp (fruiting body) development. A broad developmental grouping term. Reason: DimA affects multicellular development through its role in DIF-1 response and cell-type patterning; sorocarp development is a correct but broad developmental context term, retained as non-core. Supporting Evidence: PMID:14729573 the dimA(-) mutant exhibits cell autonomous |
| GO:0006935 chemotaxis | IMP PMID:16234315 Microarray phenotyping in Dictyostelium reveals a regulon of... | KEEP AS NON CORE | Summary: This annotation derives from a large-scale microarray phenotyping study that identified a co-regulated regulon of chemotaxis genes and tested mutants for chemotaxis defects. The cached record is abstract-only and does not describe dimA specifically, but the dictyBase IMP annotation implies a measured chemotaxis phenotype. Chemotaxis is peripheral to DimA's role as a DIF-1-responsive transcription factor. Reason: A chemotaxis phenotype for dimA was inferred from a co-expression/mutant phenotyping screen and is a pleiotropic, non-core role relative to DimA's central function in DIF-1 signalling and cell-type differentiation. Supporting Evidence: PMID:16234315 Six mutants exhibited chemotaxis defects |
| GO:0030435 sporulation resulting in formation of a cellular spore | IMP PMID:15470429 Pleiotropy as a mechanism to stabilize cooperation. | KEEP AS NON CORE | Summary: In chimaeras, loss of dimA results in exclusion of mutant cells from the spore mass, reflecting the pleiotropic linkage between DimA-dependent prestalk differentiation and spore formation. DimA thus acts upstream of spore formation, but this is a developmental/ecological consequence rather than a core molecular function. Reason: The connection to sporulation is through DimA's role in DIF-1 response and cell-fate choice (pleiotropy stabilizing cooperation), not a direct core function of the transcription factor. Retained as non-core. Supporting Evidence: PMID:15470429 lack of the dimA gene results in exclusion from spores |
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