Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0282612 (PIN)
2,291 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plant growth and development are sustained by meristems. Meristem activity is controlled by auxin and cytokinin, two hormones whose interactions in determining a specific developmental output are still poorly understood. By means of a comprehensive genetic and molecular analysis in Arabidopsis, we show that a primary cytokinin-response transcription factor, ARR1, activates the gene SHY2/IAA3 (SHY2), a repressor of auxin signaling that negatively regulates the PIN auxin transport facilitator genes: thereby, cytokinin causes auxin redistribution, prompting cell differentiation. Conversely, auxin mediates degradation of the SHY2 protein, sustaining PIN activities and cell division. Thus, the cell differentiation and division balance necessary for controlling root meristem size and root growth is the result of the interaction between cytokinin and auxin through a simple regulatory circuit converging on the SHY2 gene.
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PMID:A genetic framework for the control of cell division and differentiation in the root meristem. 1903 36

Upon seed germination, apical meristems grow as cell division prevails over differentiation and reach their final size when division and differentiation reach a balance. In the Arabidopsis root meristem, this balance results from the interaction between cytokinin (promoting differentiation) and auxin (promoting division) through a regulatory circuit whereby the ARR1 cytokinin-responsive transcription factor activates the gene SHY2, which negatively regulates the PIN genes encoding auxin transport facilitators. However, it remains unknown how the final meristem size is set, i.e., how a change in the relative rates of cell division and differentiation is brought about to cause meristem growth to stop. Here, we show that during meristem growth, expression of SHY2 is driven by another cytokinin-response factor, ARR12, and that completion of growth is brought about by the upregulation of SHY2 caused by both ARR12 and ARR1: this leads to an increase in cell differentiation rate that balances it with division, thus setting root meristem size. We also show that gibberellins selectively repress expression of ARR1 at early stages of meristem development, and that the DELLA protein REPRESSOR OF GA 1-3 (RGA) mediates this negative control.
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PMID:The rate of cell differentiation controls the Arabidopsis root meristem growth phase. 2062 Sep 2

Optimal root architecture is established by multiple intrinsic (e.g. hormones) and extrinsic (e.g. gravity and touch) signals and is established, in part, by directed root growth. We show that asymmetrical exposure of cytokinin (CK) at the root tip in Arabidopsis (Arabidopsis thaliana) promotes cell elongation that is potentiated by glucose in a hexokinase-influenced, G protein-independent manner. This mode of CK signaling requires the CK receptor, ARABIDOPSIS HISTIDINE KINASE4 and, at a minimum, its cognate type B ARABIDOPSIS RESPONSE REGULATORS ARR1, ARR10, and ARR11 for full responsiveness, while type A response regulators act redundantly to attenuate this CK response. Ethylene signaling through the ethylene receptor ETHYLENE RESISTANT1 and its downstream signaling element ETHYLENE INSENSITIVE2 are required for CK-induced root cell elongation. Negative and positive feedback loops are reinforced by CK regulation of the expression of the genes encoding these elements in both the CK and ethylene signaling pathways. Auxin transport facilitated by PIN-FORMED2 as well as auxin signaling through control of the steady-state level of transcriptional repressors INDOLE-3-ACETIC ACID7 (IAA7), IAA14, and IAA17 via TRANSPORT INHIBITOR RESPONSE1/AUXIN SIGNALING F-BOX PROTEIN are involved in CK-induced root cell elongation. This action lies downstream of ethylene and CK induction. Intrinsic signaling in this response operates independently of the extrinsic signal touch, although actin filament organization, which is important in the touch response, may be important for this response, since latrunculin B can induce similar growth. This root growth response may have adaptive significance, since CK responsiveness is inversely related to root coiling and waving, two root behaviors known to be important for fitness.
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PMID:Cytokinin interplay with ethylene, auxin, and glucose signaling controls Arabidopsis seedling root directional growth. 2166 52

Cytokinin promotes shoot branching by activating axillary buds, but its mechanism of action in Arabidopsis (Arabidopsis thaliana) in this process is unclear. We have shown previously that a hextuple mutant lacking a clade of type-A Arabidopsis Response Regulators (ARRs) known to act in cytokinin signaling has reduced shoot branching compared with the wild type. Since these proteins typically act as negative regulators of cytokinin signaling, this is an unexpected result. To explore this paradox more deeply, we characterized the effects of loss of function of the type-B ARR, ARR1, which positively regulates cytokinin-induced gene expression. The arr1 mutant has increased branching, consistent with a role antagonistic to the type-A ARRs but in apparent conflict with the known positive role for cytokinin in bud activation. We show that the arr branching phenotypes correlate with increases in stem auxin transport and steady-state levels of the auxin export proteins PIN3 and PIN7 on the plasma membrane of xylem-associated cells in the main stem. Cytokinin treatment results in an increased accumulation of PIN3, PIN7, and the closely related PIN4 within several hours, and loss of PIN3, PIN4, and PIN7 can partially rescue the arr1 branching phenotype. This suggests that there are multiple signaling pathways for cytokinin in bud outgrowth; one of these pathways regulates PIN proteins in shoots, independently of the canonical signaling function of the ARR genes tested here. A hypothesis consistent with the arr shoot phenotypes is that feedback control of biosynthesis leads to altered cytokinin accumulation, driving cytokinin signaling via this pathway.
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PMID:Cytokinin Targets Auxin Transport to Promote Shoot Branching. 2971 21