CAPRICE (CPC) is a small (94 aa) single-repeat R3-type MYB protein of Arabidopsis that lacks an R2 repeat and a transcriptional activation domain. CPC is transcribed in non-hair (atrichoblast) cells of the root epidermis under control of the WER-GL3/EGL3-TTG1 MYB-bHLH-WD40 complex, moves through plasmodesmata into neighbouring hair-position cells and accumulates in their nuclei, where it binds the bHLH proteins GL3/EGL3 and competes with the R2R3-MYB WEREWOLF. This blocks activation of GLABRA2 and allows root hair (trichoblast) fate, making CPC a positive regulator of root hair cell specification. In the shoot epidermis CPC is likewise induced by GL1-GL3 and acts with TRIPTYCHON (TRY) and other R3 MYBs (ETC1-3, TCL1) as a mobile lateral inhibitor of trichome initiation: cpc mutants have increased trichome density, try cpc double mutants form large trichome clusters, and CPC overexpression abolishes trichomes. CPC also promotes stomatal formation in the hypocotyl redundantly with TRY.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0000976 transcription cis-regulatory region binding | IBA GO_REF:0000033 | MARK AS OVER ANNOTATED | Summary: IBA cis-regulatory region binding from the deep MYB-domain node shared with R2R3 MYBs. Reason: CPC is a truncated single-repeat MYB without an R2 repeat; no direct DNA binding by CPC has been demonstrated, and its mechanism is competitive binding to GL3/EGL3 that prevents formation of the active WER/GL1-bHLH-TTG1 complex. The DNA-binding activity inherited from the R2R3-MYB ancestor is unlikely to be retained in a functionally meaningful form. Propagation Review Root cause: PROPAGATION BAD Failure modes: FUNCTIONAL DIVERGENCE ROLE CONFLATION Sources checked: PANTHER:PTN000067606 · PTN000067606 SUPPORTS SOURCE BUT NOT TARGET Deep MYB node seeded by R2R3 MYBs (e.g. AT5G40330, AT1G66230) and TRY; CPC retains only the R3 repeat and acts by bHLH competition. Supporting Evidence: PMID:21914815 WER and CPC compete with one another to define cell fates in the Arabidopsis root epidermis file:ARATH/CPC/CPC-deep-research-falcon.md Domain similarity alone does not establish that CPC directly binds target DNA |
| GO:0003700 DNA-binding transcription factor activity | ISS PMID:11118137 Arabidopsis transcription factors: genome-wide comparative a... | MODIFY | Summary: ISS DNA-binding transcription factor activity from the genome-wide TF survey. Reason: The Myb-like domain suggested a transcription factor, but CPC lacks an activation domain and acts by binding GL3/EGL3 and competing with WER/GL1. Replace with transcription regulator inhibitor activity. Proposed replacements: transcription regulator inhibitor activity Supporting Evidence: PMID:14627722 they interact with the incomplete MYB protein CPC in the H position, which blocks the non-hair pathway and leads to the hair cell fate PMID:21914815 WER and CPC compete with one another to define cell fates in the Arabidopsis root epidermis |
| GO:0003700 DNA-binding transcription factor activity | ISS PMID:9262483 Epidermal cell differentiation in Arabidopsis determined by ... | MODIFY | Summary: ISS from the CPC cloning paper, based on the Myb-like DNA-binding domain. Reason: Sequence-based inference from the MYB repeat; subsequent work showed CPC acts as a competitive inhibitor of the bHLH partners rather than as a DNA-binding activator. Proposed replacements: transcription regulator inhibitor activity Supporting Evidence: PMID:9262483 The mutated gene CAPRICE (CPC) encoded a protein with a Myb-like DNA binding domain typical of transcription factors involved in animal and plant development. PMID:12403712 We also show that the N terminus of bHLH protein interacts with CPC and is responsible for the GL2 expression. |
| GO:0005515 protein binding | IPI PMID:12917293 A network of redundant bHLH proteins functions in all TTG1-d... | MODIFY | Summary: Y2H/overexpression: CPC interacts with EGL3. Reason: Protein binding is uninformative. CPC's binding to the bHLH proteins GL3/EGL3 is precisely the mechanism by which it inhibits the WER/GL1-containing activator complex, so the evidence-backed informative term is transcription regulator inhibitor activity. Proposed replacements: transcription regulator inhibitor activity Supporting Evidence: PMID:12917293 Yeast two-hybrid and plant overexpression studies show that EGL3, like GL3, interacts with TTG1, the myb proteins GL1, PAP1 and 2, CPC and TRY, and it will form heterodimers with GL3. |
| GO:0005515 protein binding | IPI PMID:14627722 The bHLH genes GLABRA3 (GL3) and ENHANCER OF GLABRA3 (EGL3) ... | MODIFY | Summary: Y2H: CPC interacts with EGL3 (root epidermal patterning). Reason: Protein binding is uninformative. CPC's binding to the bHLH proteins GL3/EGL3 is precisely the mechanism by which it inhibits the WER/GL1-containing activator complex, so the evidence-backed informative term is transcription regulator inhibitor activity. Proposed replacements: transcription regulator inhibitor activity Supporting Evidence: PMID:14627722 they interact with the incomplete MYB protein CPC in the H position, which blocks the non-hair pathway and leads to the hair cell fate |
| GO:0005515 protein binding | IPI PMID:15361138 Comprehensive identification of Arabidopsis thaliana MYB tra... | MODIFY | Summary: Systematic MYB-bHLH interaction screen: CPC with EGL3 via the R3 bHLH-interaction motif. Reason: Protein binding is uninformative. CPC's binding to the bHLH proteins GL3/EGL3 is precisely the mechanism by which it inhibits the WER/GL1-containing activator complex, so the evidence-backed informative term is transcription regulator inhibitor activity. The cached PMID:15361138 record is abstract-only (it states the shared R3 interaction signature but names no pairs), so the per-pair interaction data are in the full text, which we defer to the curator on. Proposed replacements: transcription regulator inhibitor activity Supporting Evidence: PMID:15361138 as the structural basis for interaction between MYB and R/B-like BHLH proteins |
| GO:0005634 nucleus | IBA GO_REF:0000033 | ACCEPT | Summary: IBA nucleus. Reason: CPC accumulates in trichoblast nuclei. Supporting Evidence: PMID:16291794 CPC is transported from atrichoblasts (hairless cells), where it is expressed, to trichoblasts, and generally accumulates in their nuclei. |
| GO:0005634 nucleus | IDA PMID:16291794 Cell-to-cell movement of the CAPRICE protein in Arabidopsis ... | ACCEPT | Summary: IDA: CPC-GFP accumulates in nuclei of hair-forming cells after moving from non-hair cells. Reason: Direct localization evidence. Supporting Evidence: PMID:16291794 CPC is transported from atrichoblasts (hairless cells), where it is expressed, to trichoblasts, and generally accumulates in their nuclei. |
| GO:0005634 nucleus | IDA PMID:16581911 Transcriptional and posttranscriptional regulation of transc... | ACCEPT | Summary: IDA from a systematic GFP reporter study of root transcription factors (CPC among the mobile TFs). Reason: Consistent with CPC-specific localization data; abstract-only cache, so deferring to the curator. Supporting Evidence: PMID:16581911 via intercellular protein movement (6/24) |
| GO:0005634 nucleus | IEA GO_REF:0000044 | ACCEPT | Summary: IEA nucleus from UniProt subcellular location. Reason: Consistent with experimental localization. Supporting Evidence: PMID:16291794 CPC is transported from atrichoblasts (hairless cells), where it is expressed, to trichoblasts, and generally accumulates in their nuclei. |
| GO:0005634 nucleus | ISM GO_REF:0000122 | ACCEPT | Summary: ISM (AtSubP) nucleus. Reason: Consistent with experimental localization. Supporting Evidence: PMID:16291794 CPC is transported from atrichoblasts (hairless cells), where it is expressed, to trichoblasts, and generally accumulates in their nuclei. |
| GO:0006355 regulation of DNA-templated transcription | IBA GO_REF:0000033 | ACCEPT | Summary: IBA regulation of DNA-templated transcription. Reason: CPC represses GL2 transcription indirectly by inhibiting the MBW activator complex. Supporting Evidence: PMID:12403712 CPC protein moves to the hair-forming cells and represses the GL2 expression |
| GO:0009653 anatomical structure morphogenesis | IEA GO_REF:0000117 | MARK AS OVER ANNOTATED | Summary: IEA (ARBA) anatomical structure morphogenesis. Reason: CPC acts in epidermal cell fate specification, not in morphogenesis of an anatomical structure; the term is too broad to be informative and misplaces the role. Supporting Evidence: PMID:9262483 Thus, the CPC gene determines the fate of epidermal cell differentiation in Arabidopsis. |
| GO:0010063 positive regulation of trichoblast fate specification | IMP PMID:11326047 Evolution and genetics of root hair stripes in the root epid... | ACCEPT | Summary: IMP: CPC is required for hair cell development in the root epidermis. Reason: cpc mutants have few root hairs and CPC overexpression produces extra root hairs; CPC promotes trichoblast fate by blocking GL2 activation in H-position cells. Supporting Evidence: PMID:11326047 CAPRICE (CPC) is required for hair cell development PMID:9262483 Transgenic plants overexpressing CPC had more root hairs and fewer trichomes than normal. |
| GO:0010376 stomatal complex formation | IMP PMID:19513241 CAPRICE positively regulates stomatal formation in the Arabi... | KEEP AS NON CORE | Summary: IMP: CPC promotes stomatal formation in the hypocotyl redundantly with TRY. Reason: Experimentally supported, but a secondary context of the same epidermal patterning mechanism. Supporting Evidence: PMID:19513241 CPC protein might move to the nucleus of neighbouring stoma-forming cells, where it promotes stomata formation in a redundant manner with TRIPTYCHON (TRY) |
| GO:0030154 cell differentiation | IBA GO_REF:0000033 | MODIFY | Summary: IBA cell differentiation. Reason: Correct but very general; CPC acts specifically in plant epidermal cell differentiation (root hair, trichome, stomata). Propagation Review Root cause: TERM SCOPING PROBLEM Failure modes: GRANULARITY MISMATCH Proposed replacements: plant epidermal cell differentiation Supporting Evidence: PMID:9262483 Thus, the CPC gene determines the fate of epidermal cell differentiation in Arabidopsis. |
| GO:0030154 cell differentiation | TAS PMID:9262483 Epidermal cell differentiation in Arabidopsis determined by ... | MODIFY | Summary: TAS cell differentiation from the CPC cloning paper. Reason: As for the IBA row; the paper describes epidermal cell differentiation specifically. Proposed replacements: plant epidermal cell differentiation Supporting Evidence: PMID:9262483 Thus, the CPC gene determines the fate of epidermal cell differentiation in Arabidopsis. |
| GO:0048731 system development | IEA GO_REF:0000117 | MARK AS OVER ANNOTATED | Summary: IEA (ARBA) system development. Reason: Uninformative high-level term; more specific epidermal terms capture CPC's role. Supporting Evidence: PMID:9262483 Thus, the CPC gene determines the fate of epidermal cell differentiation in Arabidopsis. |
| GO:0090558 plant epidermis development | IEA GO_REF:0000117 | KEEP AS NON CORE | Summary: IEA (ARBA) plant epidermis development. Reason: Correct general context; the specific cell fate roles are captured elsewhere. Supporting Evidence: PMID:9262483 Thus, the CPC gene determines the fate of epidermal cell differentiation in Arabidopsis. |
| GO:0090627 plant epidermal cell differentiation | IEA GO_REF:0000117 | ACCEPT | Summary: IEA (ARBA) plant epidermal cell differentiation. Reason: Consistent with CPC's experimentally established role. Supporting Evidence: PMID:9262483 Thus, the CPC gene determines the fate of epidermal cell differentiation in Arabidopsis. |
| GO:0090627 plant epidermal cell differentiation | IMP PMID:12403712 Role of a positive regulator of root hair development, CAPRI... | ACCEPT | Summary: IMP: CPC moves to hair-forming cells, represses GL2 and promotes hair cell differentiation. Reason: Direct experimental support. Supporting Evidence: PMID:12403712 CPC protein moves to the hair-forming cells and represses the GL2 expression |
| GO:1900032 regulation of trichome patterning | IMP PMID:12356720 TRIPTYCHON and CAPRICE mediate lateral inhibition during tri... | NEW | Summary: CPC acts with TRY as a mobile lateral inhibitor in leaf trichome spacing; try cpc double mutants convert all cells contacting a trichome into trichomes. Reason: CPC itself performs the inhibitory step of the patterning mechanism (binding GL3 and competing with GL1 in neighbouring cells), so this is participation rather than mere necessity. Comparator: the paralog TRY carries GO:1900032 by IMP in GOA (PMID:21951724). Not an ancestor/descendant of other CPC terms. Supporting Evidence: PMID:12356720 Both genes are expressed in trichomes and act together during lateral inhibition. PMID:12356720 In try cpc double mutants, all cells in immediate contact with an already existing trichome started to bulge out and developed into trichomes PMID:12356720 An attractive explanation for this finding is that CPC competes with the R gene homolog GL3 in Arabidopsis and, depending on their balance, trichome cell fate is promoted when more GL3 is available, while an excess of CPC promotes the epidermal cell fate. |
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Download this section (compressed HTML)Q: Does CPC retain any sequence-specific DNA-binding capacity with its single R3 repeat, or is its activity entirely through bHLH sequestration/competition?
Experiment: EMSA/DAP-seq with recombinant CPC alone versus CPC-GL3 heterocomplex, compared with WER-GL3, on GL2 promoter fragments.
Hypothesis: CPC alone does not bind GL2 promoter DNA, and CPC-GL3 complexes bind with reduced affinity relative to WER-GL3.
Type: In vitro DNA binding
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