DimB is a basic-region leucine-zipper (bZIP) transcription factor that acts as a direct effector of the polyketide morphogen DIF-1 during Dictyostelium multicellular development. In unstimulated cells DimB is distributed through the cytoplasm, but exposure to DIF-1 triggers its rapid accumulation in the nucleus, where it binds sequence-specific cis-regulatory elements in target promoters. DimB can bind DNA as a homodimer and as a heterodimer with the related bZIP factor DimA. It functions as a dual-mode regulator that directly activates prestalk/basal-disc genes such as ecmB in pstB cells, spatially restricts expression of the prestalk gene ecmA, and directly represses prespore genes such as pspA. Through these activities DimB controls prestalk cell-type patterning, pstB/basal-disc and anterior-like-cell differentiation, and the choice between stalk and spore fate. Loss of DimB produces abnormally long, thin slugs and defective culmination.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0005634 nucleus | IBA GO_REF:0000033 | ACCEPT | Summary: Phylogenetic inference that DimB acts in the nucleus is consistent with direct experimental evidence that DimB accumulates in the nucleus upon DIF-1 stimulation and binds target promoters there. This is a core location. Reason: Nuclear localization is directly demonstrated for DimB and is where its transcription factor activity is exerted; the IBA inference is fully corroborated. Supporting Evidence: PMID:16410410 In the absence of DIF-1, GFP was fairly uniformly distributed throughout the cells. However, after DIF-1 treatment, both DimA:GFP and DimB:GFP exhibited nuclear accumulation |
| GO:0010468 regulation of gene expression | IBA GO_REF:0000033 | ACCEPT | Summary: DimB regulates expression of multiple developmental genes (activating ecmB, repressing pspA and others). This general parent term is correct but a more specific descendant (regulation of DNA-templated transcription) better captures its mechanism. Reason: The annotation is accurate as a broad statement of DimB's function as a transcriptional regulator; more specific transcription terms are also present. Supporting Evidence: PMID:22253818 In response to the signaling polyketide DIF-1 DimB directly activates transcription of the ecmB gene in pstB cells |
| GO:0043565 sequence-specific DNA binding | IBA GO_REF:0000033 | ACCEPT | Summary: DimB was purified by affinity chromatography on ecmA promoter fragments and binds defined sites in the ecmA, ecmB and pspA promoters, directly demonstrating sequence-specific DNA binding. The IBA inference is well supported. Reason: Sequence-specific DNA binding is a core molecular function of DimB, confirmed by direct experimental evidence. Supporting Evidence: PMID:16396914 We have purified a novel bZIP transcription factor, DimB, by affinity chromatography on two spatially separated ecmA promoter fragments |
| GO:0003700 DNA-binding transcription factor activity | IEA GO_REF:0000002 | ACCEPT | Summary: InterPro2GO inference from the bZIP domain. DimB is experimentally a DNA-binding transcription factor that both activates and represses target genes, so this is a correct core molecular function. Reason: The bZIP domain-based inference matches the demonstrated function of DimB as a sequence-specific transcription factor regulating prestalk and prespore genes. Supporting Evidence: PMID:22253818 In response to the signaling polyketide DIF-1 DimB directly activates transcription of the ecmB gene in pstB cells |
| GO:0005634 nucleus | IEA GO_REF:0000044 | ACCEPT | Summary: UniProt subcellular-location mapping to nucleus, corroborated by direct experimental evidence of DIF-1-induced nuclear accumulation. Reason: Nuclear localization is a core, experimentally established location for DimB. Supporting Evidence: PMID:16410410 In the absence of DIF-1, GFP was fairly uniformly distributed throughout the cells. However, after DIF-1 treatment, both DimA:GFP and DimB:GFP exhibited nuclear accumulation |
| GO:0006355 regulation of DNA-templated transcription | IEA GO_REF:0000002 | ACCEPT | Summary: InterPro2GO inference consistent with DimB's demonstrated role as a direct transcriptional activator and repressor of developmental genes. Reason: DimB directly regulates transcription of ecmB (activation) and pspA (repression); this term accurately captures the process. Supporting Evidence: PMID:22253818 In response to the signaling polyketide DIF-1 DimB directly activates transcription of the ecmB gene in pstB cells |
| GO:0010629 negative regulation of gene expression | IMP PMID:20300194 BTG interacts with retinoblastoma to control cell fate in Di... | ACCEPT | Summary: In dimB-null cells the ALC-marker gene btg is over-induced during development, indicating that DimB normally represses btg as part of the DIF signalling response. Supports negative regulation of gene expression. Reason: Direct genetic evidence (mutant phenotype) shows DimB negatively regulates btg expression during development. Supporting Evidence: PMID:20300194 btg is overinduced in the DIF unresponsive mutants |
| GO:0043069 negative regulation of programmed cell death | IMP PMID:16410410 bZIP transcription factor interactions regulate DIF response... | KEEP AS NON CORE | Summary: In an 8-Br-cAMP monolayer assay, DIF-1-treated dimB-null cells undergo non-vacuolar cell death (NVCD) that is normally suppressed by DimB, which instead directs vacuolised stalk-cell formation. This is a genuine but downstream developmental consequence rather than a core molecular function. Reason: DimB is required to repress NVCD in the stalk differentiation pathway, so the annotation is supported, but it reflects a cell-fate outcome of DimB's transcriptional activity rather than its direct function. Supporting Evidence: PMID:16410410 NVCD is repressed by DimB |
| GO:1903014 cellular response to differentiation-inducing factor 1 | HDA PMID:25518940 The Dictyostelium prestalk inducer differentiation-inducing ... | ACCEPT | Summary: DimB is a direct effector of DIF-1 that accumulates in the nucleus and is phosphorylated in response to DIF-1. This term accurately captures DimB's role in the cellular response to the DIF-1 morphogen. Reason: DimB nuclear accumulation and phosphorylation are direct, rapid responses to DIF-1, placing DimB centrally in the cellular DIF-1 response. Supporting Evidence: PMID:25518940 DimB accumulates in the nuclei of cells induced with DIF-1 and is phosphorylated |
| GO:0031153 slug development involved in sorocarp development | IMP PMID:16396914 The Dictyostelium bZIP transcription factor DimB regulates p... | KEEP AS NON CORE | Summary: dimB-null development proceeds normally to the finger stage, then produces extremely long, thin fingers/slugs, implicating DimB in normal slug morphogenesis. This is a downstream developmental phenotype. Reason: The mutant slug phenotype supports a role in slug development, but this is an organismal-level consequence of DimB's transcriptional activity rather than its core molecular function. Supporting Evidence: PMID:16396914 DimB is not essential for normal expression of the ecmA gene, instead it spatially limits its expression |
| GO:0005634 nucleus | IDA PMID:16396914 The Dictyostelium bZIP transcription factor DimB regulates p... | ACCEPT | Summary: Direct evidence that DimB rapidly accumulates in the nucleus upon DIF-1 exposure and associates with the ecmA promoter there. Core active location. Reason: Nuclear localization where DimB exerts its transcription factor activity is directly demonstrated. Supporting Evidence: PMID:16396914 DimB rapidly accumulates in the nucleus when cells are exposed to DIF-1 |
| GO:0005634 nucleus | IDA PMID:16410410 bZIP transcription factor interactions regulate DIF response... | ACCEPT | Summary: Direct GFP-localization evidence shows DimB accumulates in the nucleus after DIF-1 treatment. Core active location. Reason: Independent direct evidence confirms nuclear localization as the site of DimB action. Supporting Evidence: PMID:16410410 In the absence of DIF-1, GFP was fairly uniformly distributed throughout the cells. However, after DIF-1 treatment, both DimA:GFP and DimB:GFP exhibited nuclear accumulation |
| GO:0005634 nucleus | IDA PMID:21458438 DIF-1 regulates Dictyostelium basal disc differentiation by ... | ACCEPT | Summary: DimB is specifically nuclear enriched in pstB cells during normal development, where it activates basal-disc gene expression. Core active location. Reason: Direct evidence places active DimB in the nucleus of the responding cells. Supporting Evidence: PMID:21458438 DimB is specifically nuclear enriched in the pstB cells |
| GO:0005737 cytoplasm | IDA PMID:16396914 The Dictyostelium bZIP transcription factor DimB regulates p... | KEEP AS NON CORE | Summary: In the absence of DIF-1, DimB is distributed through the cytoplasm and only translocates to the nucleus upon DIF-1 stimulation. Cytoplasmic localization reflects the inactive/resting state rather than the functional compartment. Reason: The cytoplasmic pool is the pre-stimulation reservoir; DimB's functional compartment is the nucleus. The localization is real but not the core site of action. Supporting Evidence: PMID:16410410 In the absence of DIF-1, GFP was fairly uniformly distributed throughout the cells. However, after DIF-1 treatment, both DimA:GFP and DimB:GFP exhibited nuclear accumulation |
| GO:0031287 positive regulation of sorocarp stalk cell differentiation | IMP PMID:16396914 The Dictyostelium bZIP transcription factor DimB regulates p... | KEEP AS NON CORE | Summary: DimB promotes prestalk/basal-disc differentiation, and dimB-null cells fail to make stalk cells in response to DIF-1. This is a genuine developmental role, but a downstream outcome of DimB's transcriptional activity. Reason: Supported by mutant phenotype (loss of DIF-1-induced stalk differentiation), but represents an organismal cell-differentiation outcome rather than DimB's core molecular function. Supporting Evidence: PMID:21458438 leading to nuclear localization of DimB and direct activation of cell type-specific gene expression |
| GO:0043565 sequence-specific DNA binding | IDA PMID:16396914 The Dictyostelium bZIP transcription factor DimB regulates p... | ACCEPT | Summary: DimB was purified by affinity chromatography on ecmA promoter fragments, directly demonstrating sequence-specific DNA binding. Core molecular function. Reason: Direct biochemical evidence for sequence-specific promoter binding. Supporting Evidence: PMID:16396914 We have purified a novel bZIP transcription factor, DimB, by affinity chromatography on two spatially separated ecmA promoter fragments |
| GO:0045184 establishment of protein localization | IMP PMID:16410410 bZIP transcription factor interactions regulate DIF response... | KEEP AS NON CORE | Summary: DimB is required for DIF-1-induced nuclear accumulation of its partner DimA; in dimB-null cells DimA fails to accumulate in the nucleus. The annotation captures this regulatory effect but with a very general term. Reason: Supported by direct genetic evidence that DimB controls DimA nuclear localization, but this is a specialized downstream effect and the term is broad; not a core function. Supporting Evidence: PMID:16410410 nuclear accumulation of DimA in response to DIF-1 is dependent on DimB |
| GO:0005737 cytoplasm | IDA PMID:16410410 bZIP transcription factor interactions regulate DIF response... | KEEP AS NON CORE | Summary: Consistent with the other cytoplasm annotation, DimB:GFP is uniformly distributed (including cytoplasm) before DIF-1 and translocates to the nucleus after stimulation. Reason: Cytoplasmic localization is the resting-state distribution; the functional compartment is the nucleus. Supporting Evidence: PMID:16410410 In the absence of DIF-1, GFP was fairly uniformly distributed throughout the cells. However, after DIF-1 treatment, both DimA:GFP and DimB:GFP exhibited nuclear accumulation |
| GO:0005515 protein binding | IPI PMID:16410410 bZIP transcription factor interactions regulate DIF response... | MODIFY | Summary: This IPI annotation records the physical interaction of DimB with the bZIP factor DimA (UniProtKB:Q54XG7). Bare protein binding is uninformative; the interaction is bZIP heterodimerization, better captured by protein heterodimerization activity. Reason: Pull-down assays show DimB forms heterodimeric complexes with DimA in vitro. Replacing the generic term with protein heterodimerization activity conveys the mechanistic nature (bZIP leucine-zipper dimerization) of the interaction. Proposed replacements: protein heterodimerization activity Supporting Evidence: PMID:16410410 Pull-down assays with purified proteins showed that DimA and DimB can form homodimeric and heterodimeric complexes in vitro PMID:16410410 a second bZIP transcription factor (DimB) that can directly interact with DimA in vitro |
| GO:0000976 transcription cis-regulatory region binding | IDA PMID:21458438 DIF-1 regulates Dictyostelium basal disc differentiation by ... | ACCEPT | Summary: ChIP analysis directly shows DimB binding to the ecmB cis-regulatory region (promoter) in DIF-1-induced cells. Core molecular function. Reason: Direct in vivo evidence of DimB binding a defined promoter cis-regulatory region. Supporting Evidence: PMID:21458438 ChIP analysis shows that DimB binds to the ecmB promoter in DIF-induced cells |
| GO:0000976 transcription cis-regulatory region binding | IDA PMID:22253818 Transcriptional repression by a bZIP protein regulates Dicty... | ACCEPT | Summary: ChIP analysis shows DIF-1-induced binding of DimB to the pspA promoter, confirming cis-regulatory region binding at a prespore-gene promoter. Core molecular function. Reason: Independent direct in vivo evidence of DimB binding a promoter cis-regulatory region. Supporting Evidence: PMID:22253818 Thus DIF induces binding of DimB to the pspA promoter |
| GO:0010628 positive regulation of gene expression | IMP PMID:21458438 DIF-1 regulates Dictyostelium basal disc differentiation by ... | ACCEPT | Summary: DimB directly activates ecmB transcription in pstB cells; in dimB-null cells ecmB is not DIF-inducible. Supports positive regulation of gene expression. Reason: Direct activation of ecmB, supported by ChIP and mutant analysis, makes this a well-supported functional annotation. Supporting Evidence: PMID:22253818 In response to the signaling polyketide DIF-1 DimB directly activates transcription of the ecmB gene in pstB cells |
| GO:0010629 negative regulation of gene expression | IMP PMID:20080085 A new Dictyostelium prestalk cell sub-type. | ACCEPT | Summary: Genome-wide microarray analysis of dimB-null cells identified genes that become DIF-inducible only when DimB is absent, i.e. genes normally under negative control by DimB. Supports negative regulation of gene expression. Reason: Direct genetic (mutant) evidence that DimB represses a set of DIF-1 target genes. Supporting Evidence: PMID:20080085 these genes fall under negative control by the same two transcription factors |
| GO:0010629 negative regulation of gene expression | IMP PMID:22253818 Transcriptional repression by a bZIP protein regulates Dicty... | ACCEPT | Summary: DimB directly represses the prespore gene pspA; DIF-1-dependent repression of pspA is abrogated in a dimB-null strain, and DimB binds the pspA promoter. Core repressive activity. Reason: Direct in vivo binding plus mutant analysis establish DimB as a direct repressor of pspA. Supporting Evidence: PMID:22253818 DIF-1 represses pspA gene expression in a suspension cell assay but this repression is abrogated in a dimB null strain |
| GO:0042802 identical protein binding | IPI PMID:16410410 bZIP transcription factor interactions regulate DIF response... | ACCEPT | Summary: Pull-down assays show DimB can form homodimeric complexes (self- interaction; UniProtKB:Q54ER9), consistent with bZIP homodimerization. This is informative (unlike bare protein binding) and supported. Reason: Direct in vitro evidence of DimB homodimerization; retained as an informative interaction annotation reflecting bZIP dimerization behavior. Supporting Evidence: PMID:16410410 Pull-down assays with purified proteins showed that DimA and DimB can form homodimeric and heterodimeric complexes in vitro |
| GO:0030587 sorocarp development | IEP PMID:25887420 Leaps and lulls in the developmental transcriptome of Dictyo... | KEEP AS NON CORE | Summary: An IEP annotation based on dimB's developmentally regulated expression trajectory in a genome-wide transcriptome study. Expression-based inference of a broad developmental role. Reason: The developmental-transcriptome correlation is consistent with a role in sorocarp development, but this very general term rests on expression pattern rather than direct functional evidence and is not a core function. Supporting Evidence: PMID:25887420 dimB and dstC continued on a more graded trajectory |
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