RESUMEN
The phytohormone auxin controls plant growth and development via TIR1-dependent protein degradation of canonical AUX/IAA proteins, which normally repress the activity of auxin response transcription factors (ARFs). IAA33 is a non-canonical AUX/IAA protein lacking a TIR1-binding domain, and its role in auxin signaling and plant development is not well understood. Here, we show that IAA33 maintains root distal stem cell identity and negatively regulates auxin signaling by interacting with ARF10 and ARF16. IAA33 competes with the canonical AUX/IAA repressor IAA5 for binding to ARF10/16 to protect them from IAA5-mediated inhibition. In contrast to auxin-dependent degradation of canonical AUX/IAA proteins, auxin stabilizes IAA33 protein via MITOGEN-ACTIVATED PROTEIN KINASE 14 (MPK14) and does not affect IAA33 gene expression. Taken together, this study provides insight into the molecular functions of non-canonical AUX/IAA proteins in auxin signaling transduction.
Asunto(s)
Proteínas de Arabidopsis/metabolismo , Arabidopsis/metabolismo , Proteínas de Unión al ADN/metabolismo , Regulación de la Expresión Génica de las Plantas/efectos de los fármacos , Ácidos Indolacéticos/farmacología , Proteínas Nucleares/metabolismo , Plantas Modificadas Genéticamente/metabolismo , Arabidopsis/efectos de los fármacos , Arabidopsis/crecimiento & desarrollo , Proteínas de Arabidopsis/genética , Proteínas de Unión al ADN/genética , Proteínas Nucleares/genética , Fosforilación , Reguladores del Crecimiento de las Plantas/farmacología , Plantas Modificadas Genéticamente/efectos de los fármacos , Plantas Modificadas Genéticamente/crecimiento & desarrollo , Proteolisis , Transducción de SeñalRESUMEN
Pre-mRNA (messenger RNA) splicing participates in the regulation of numerous biological processes in plants. For example, alternative splicing shapes transcriptomic responses to abiotic and biotic stress, and controls developmental programs. However, no study has revealed a role for splicing in maintaining the root stem cell niche. Here, a screen for defects in root growth in Arabidopsis thaliana identified an ethyl methane sulfonate mutant defective in pre-mRNA splicing (rdm16-4). The rdm16-4 mutant displays a short-root phenotype resulting from fewer cells in the root apical meristem. The PLETHORA1 (PLT1) and PLT2 transcription factor genes are important for root development and were alternatively spliced in rdm16-4 mutants, resulting in a disordered root stem cell niche and retarded root growth. The root cap of rdm16-4 contained reduced levels of cytokinins, which promote differentiation in the developing root. This reduction was associated with the alternative splicing of genes encoding cytokinin signaling factors, such as ARABIDOPSIS HISTIDINE PHOSPHOTRANSFER PROTEIN5 and ARABIDOPSIS RESPONSE REGULATORS (ARR1, ARR2, and ARR11). Furthermore, expression of the full-length coding sequence of ARR1 or exogenous cytokinin application partially rescued the short-root phenotype of rdm16-4. This reveals that the RDM16-mediated alternative splicing of cytokinin signaling components contributes to root growth.
Asunto(s)
Proteínas de Arabidopsis/metabolismo , Proteínas Nucleares/metabolismo , Factores de Empalme de ARN/metabolismo , Células Madre/metabolismo , Factores de Transcripción/metabolismo , Proteínas de Arabidopsis/genética , Citocininas/genética , Citocininas/metabolismo , Metanosulfonato de Etilo , Regulación de la Expresión Génica de las Plantas/genética , Regulación de la Expresión Génica de las Plantas/fisiología , Meristema/genética , Meristema/metabolismo , Proteínas Nucleares/genética , Precursores del ARN/genética , Precursores del ARN/metabolismo , Factores de Empalme de ARN/genética , Factores de Transcripción/genéticaRESUMEN
Shade avoidance syndrome (SAS) arises in densely growing plants that compete for light. In Arabidopsis thaliana, phytochrome interacting factor (PIF) proteins link the perception of shade to stem elongation via auxin production. Here, we report that PIFs inhibit the shade-induced expression of AUXIN RESPONSE FACTOR 18 (ARF18), and ARF18 represses auxin signaling. Therefore, PIF-mediated inhibition of ARF18 enhances auxin-dependent hypocotyl elongation in simulated shade. Furthermore, we show that both PIFs and ARF18 directly repress qua-quine starch (QQS), which controls the allocation of carbon and nitrogen. Shade-repressed QQS attenuates the conversion of starch to protein and thus reduced leaf area. Our results suggest that PIF-dependent gene regulation coordinates multiple SAS responses, including altered stem growth via ARF18, as well as altered leaf growth and metabolism via QQS.
Asunto(s)
Proteínas de Arabidopsis , Arabidopsis , Fitocromo , Arabidopsis/genética , Arabidopsis/metabolismo , Proteínas de Arabidopsis/genética , Proteínas de Arabidopsis/metabolismo , Regulación de la Expresión Génica de las Plantas , Hipocótilo/metabolismo , Ácidos Indolacéticos , Luz , Fitocromo/metabolismoRESUMEN
Auxin plays a critical role in lateral root (LR) formation. The signaling module composed of auxin-response factors (ARFs) and lateral organ boundaries domain transcription factors mediates auxin signaling to control almost every stage of LR development. Here, we show that auxin-induced degradation of the APETALA2/Ethylene Responsive Factor (AP2/ERF) transcription factor ERF13, dependent on MITOGEN-ACTIVATED PROTEIN KINASE MPK14-mediated phosphorylation, plays an essential role in LR development. Overexpression of ERF13 results in restricted passage of the LR primordia through the endodermal layer, greatly reducing LR emergence, whereas the erf13 mutants showed an increase in emerged LR. ERF13 inhibits the expression of 3-ketoacyl-CoA synthase16 (KCS16), which encodes a fatty acid elongase involved in very-long-chain fatty acid (VLCFA) biosynthesis. Overexpression of KCS16 or exogenous VLCFA treatment rescues the LR emergence defects in ERF13 overexpression lines, indicating a role downstream of the auxin-MPK14-ERF13 signaling module. Collectively, our study uncovers a novel molecular mechanism by which MPK14-mediated auxin signaling modulates LR development via ERF13-regulated VLCFA biosynthesis.