CYCLIN D6;1 (CYCD6;1, At4g03270) is a D-type cyclin of Arabidopsis that acts as the regulatory subunit of cyclin-dependent kinases in a small set of formative (asymmetric, periclinal) cell divisions. CYCD6;1 is a direct transcriptional target of the SHORT-ROOT (SHR)-SCARECROW (SCR) complex: its promoter is bound by SHR and SCR and is switched on in the cortex/endodermis initial (CEI) and its daughter at the onset of the division that separates the endodermis and cortex layers, and later in a subset of endodermal cells that form middle cortex and in lateral root primordia. Expression is enhanced by auxin in a SHR/SCR-dependent manner, restricted by RETINOBLASTOMA-RELATED (RBR) and repressed by NAC1-TOPLESS. CYCD6;1 binds and stimulates B-type CDKs (CDKB1;1/CDKB1;2), and the CYCD6;1-CDKB1 kinase phosphorylates RBR, relieving RBR inhibition of SCR and so forming a feed-forward loop that positions the asymmetric division. The protein is found in the nucleus and cytoplasm and is turned over by the proteasome. cycd6;1 mutants show fewer CEI-daughter periclinal divisions and reduced middle-cortex formation without general proliferation defects, and ectopic CYCD6;1 partially restores formative divisions in shr.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0000082 G1/S transition of mitotic cell cycle | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: Phylogenetic inference of a G1/S role for D-type cyclins. Reason: CYCD6;1-CDKB1 phosphorylates RBR, the canonical G1/S gatekeeper, so the inference is plausible; however CYCD6;1 is dedicated to specific formative divisions rather than general cell-cycle progression, and a direct G1/S role has not been shown. Supporting Evidence: PMID:22921914 Based on our genetic and biochemical data, RBR phosphorylation is carried out by a complex of CYCD6;1 with either CDKB1;1 or CDKB1;2 PMID:20596025 These results indicate that CYCD6;1 is not required for proliferative cell divisions but is specifically involved in formative divisions needed for proper ground tissue patterning |
| GO:0000307 cyclin-dependent protein kinase holoenzyme complex | IBA GO_REF:0000033 | ACCEPT | Summary: Phylogenetic inference of membership in CDK holoenzyme complexes. Reason: CYCD6;1 forms an active kinase complex with CDKB1;1/CDKB1;2. Supporting Evidence: PMID:22921914 Based on our genetic and biochemical data, RBR phosphorylation is carried out by a complex of CYCD6;1 with either CDKB1;1 or CDKB1;2 PMID:22921914 revealed that CYCD6;1 binding increased basal activity of CDKB1 |
| GO:0005515 protein binding | IPI PMID:20706207 Targeted interactomics reveals a complex core cell cycle mac... | REMOVE | Summary: TAP co-purification with the CDK inhibitor KRP7 (AT1G49620). Reason: Removed under the bare protein-binding policy, because the term carries no functional information. The interaction is not in doubt; ICK/KRP inhibitors can bind D-type cyclins directly through their C-terminal domain. TAP-MS resolves complex membership rather than binary contacts, so the row records co-membership of a CDK-cyclin-KRP complex. That membership is captured by the CDK holoenzyme complex annotation, and the inhibitory relationship belongs on the KRP (cyclin-dependent protein kinase inhibitor activity), not as protein binding on the cyclin. Supporting Evidence: PMID:20706207 bait–prey interactions discovered by TAP that were negative in this split-LUC assay might represent indirect interactions |
| GO:0005515 protein binding | IPI PMID:20706207 Targeted interactomics reveals a complex core cell cycle mac... | REMOVE | Summary: TAP co-purification with CKS1 (AT2G27960). Reason: Removed under the bare protein-binding policy, because the term carries no functional information. CKS proteins are scaffold subunits that dock on the CDK, and every CDK-cyclin core complex in this TAP dataset co-purified a CKS protein, so the association reflects co-membership of the CDK holoenzyme (already captured by the complex annotation) rather than a cyclin-specific binary contact. Supporting Evidence: PMID:20706207 All CDK–cyclin core complexes copurify at least one of the two scaffold CDK subunit (CKS) proteins |
| GO:0005515 protein binding | IPI PMID:20706207 Targeted interactomics reveals a complex core cell cycle mac... | REMOVE | Summary: TAP co-purification with the CDK inhibitor KRP4 (AT2G32710). Reason: Removed under the bare protein-binding policy, for the same reasons as KRP7. The association is not doubted, and KRPs can bind D-type cyclins directly, but bare protein binding from complex-level TAP-MS carries no functional information. Complex membership is captured by the CDK holoenzyme complex annotation, and the inhibition belongs on the KRP side. Supporting Evidence: PMID:20706207 bait–prey interactions discovered by TAP that were negative in this split-LUC assay might represent indirect interactions |
| GO:0005515 protein binding | IPI PMID:20706207 Targeted interactomics reveals a complex core cell cycle mac... | MODIFY | Summary: TAP co-purification with CDKA;1 (AT3G48750). Reason: The cyclin-CDK interaction is the functional basis of cyclin regulatory activity; cyclin-dependent protein serine/threonine kinase regulator activity describes it. In planta the functionally relevant partners appear to be CDKB1;1/CDKB1;2. Proposed replacements: cyclin-dependent protein serine/threonine kinase regulator activity Supporting Evidence: PMID:20706207 D-type cyclins and S-phase-specific A-type cyclins seem to be associated exclusively with CDKA;1 PMID:22921914 revealed that CYCD6;1 binding increased basal activity of CDKB1 PMID:22921914 observed specific interaction between CDKB1 and CYCD6;1 proteins |
| GO:0005634 nucleus | IBA GO_REF:0000033 | ACCEPT | Summary: Phylogenetic nuclear inference. Reason: CYCD6;1-YFP is nuclear in endodermal cells and forms nuclear complexes. Supporting Evidence: PMID:22921914 fluorescence was detected in the nucleus of some endodermis cells and in the cytoplasm of others PMID:26379676 presence of GFP fluorescence was observed only in the nucleus when the formation of complexes between PCNA1/2 and CycD4;1, CycD5;1, CycD6;1, or CycD7;1 was tested |
| GO:0005634 nucleus | ISM GO_REF:0000122 | ACCEPT | Summary: AtSubP nuclear prediction. Reason: Corroborated experimentally. Supporting Evidence: PMID:22921914 fluorescence was detected in the nucleus of some endodermis cells and in the cytoplasm of others |
| GO:0005737 cytoplasm | IBA GO_REF:0000033 | ACCEPT | Summary: Phylogenetic cytoplasmic inference. Reason: CYCD6;1-YFP is cytoplasmic in a subset of endodermal cells. Supporting Evidence: PMID:22921914 fluorescence was detected in the nucleus of some endodermis cells and in the cytoplasm of others |
| GO:0010440 stomatal lineage progression | IEA GO_REF:0000117 | REMOVE | Summary: ARBA electronic inference of stomatal lineage progression. Reason: No evidence links CYCD6;1 to the stomatal lineage; its expression and function are confined to root ground-tissue formative divisions and lateral root primordia. This appears to be an over-propagation of a D-type cyclin rule. Supporting Evidence: PMID:20596025 These results indicate that CYCD6;1 is not required for proliferative cell divisions but is specifically involved in formative divisions needed for proper ground tissue patterning PMID:20596025 In older plants, expression of pCYCD6;1::GFP was detected in lateral root primordia |
| GO:0016538 cyclin-dependent protein serine/threonine kinase regulator activity | IBA GO_REF:0000033 | ACCEPT | Summary: Phylogenetic inference of CDK regulator activity. Reason: CYCD6;1 binds CDKB1 and increases its kinase activity toward RBR; core function. Supporting Evidence: PMID:22921914 revealed that CYCD6;1 binding increased basal activity of CDKB1 PMID:22921914 Based on our genetic and biochemical data, RBR phosphorylation is carried out by a complex of CYCD6;1 with either CDKB1;1 or CDKB1;2 |
| GO:0090511 periclinal cell division | IMP PMID:20596025 Spatiotemporal regulation of cell-cycle genes by SHORTROOT l... | NEW | Summary: cycd6;1 mutants show fewer periclinal formative divisions of the CEI daughter and fewer middle-cortex divisions; ectopic CYCD6;1 promotes them. Reason: CYCD6;1 participates directly as the regulatory subunit of the CDK that drives these divisions (it does work in the process, not merely being required). No BP annotation from these studies is in GOA. Supporting Evidence: PMID:20596025 cycd6;1 CEI-daughter cells showed significantly fewer periclinal divisions than wild type at both early heart and torpedo embryo stages PMID:20596025 In wild type, middle cortex divisions were observed in 52% of roots, as compared to 12% in cycd6;1 PMID:20596025 Both CYCD6;1 and CDKB2;1 were able to partially complement the shr formative division phenotype |
| GO:0008356 asymmetric cell division | IMP PMID:22921914 A bistable circuit involving SCARECROW-RETINOBLASTOMA integr... | NEW | Summary: CYCD6;1-CDKB1 phosphorylation of RBR feeds forward with SCR to position the asymmetric divisions of the stem cell area. Reason: The formative divisions are asymmetric (the CEI daughter gives rise to endodermis plus cortex). CYCD6;1 is the cyclin subunit of the CDKB1 kinase whose RBR phosphorylation executes and positions these divisions, so the gene product does some of the work of the process itself. It is not merely required for it. GO:0008356 is not an ancestor or descendant of the periclinal cell division term also proposed here (GO:0090511 is_a GO:0051301 cell division), so the two are not redundant. Supporting Evidence: PMID:22921914 We demonstrate that this interaction, together with the activity of the RBR regulator CYCD6;1, defines the precise position of ACDs in the stem cell area through two nested feedforward loops PMID:20596025 These results indicate that CYCD6;1 is not required for proliferative cell divisions but is specifically involved in formative divisions needed for proper ground tissue patterning |
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Download this section (compressed HTML)Q: Which RBR phosphosites does CYCD6;1-CDKB1 target, and is relief of RBR-SCR binding sufficient to explain the feed-forward positioning of the formative division?
Q: Which other D-type cyclins provide the redundancy implied by the milder cycd6;1 phenotype compared with shr?
Experiment: Compare formative divisions in cycd6;1 combined with other CYCD mutants, and express a CDKB1-binding-deficient CYCD6;1 in the CEI to test whether kinase activation is required.
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