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TIR1 auxin receptors are implicated in the differential response to 4-Cl-IAA and IAA in developing pea fruit
The auxins indole-3-acetic acid (IAA) and 4-chloroindole-3-acetic acid (4-Cl-IAA) occur naturally in pea (Pisum sativum); however, only 4-Cl-IAA mimics the presence of seeds in stimulating pericarp growth. To examine if this differential auxin effect is mediated through TIR1/AFB auxin receptors, pea...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6382345/ https://www.ncbi.nlm.nih.gov/pubmed/30715391 http://dx.doi.org/10.1093/jxb/ery456 |
Sumario: | The auxins indole-3-acetic acid (IAA) and 4-chloroindole-3-acetic acid (4-Cl-IAA) occur naturally in pea (Pisum sativum); however, only 4-Cl-IAA mimics the presence of seeds in stimulating pericarp growth. To examine if this differential auxin effect is mediated through TIR1/AFB auxin receptors, pea TIR1 and AFB2 homologs were functionally characterized in Arabidopsis, and receptor expression, and auxin distribution and action were profiled in developing pea fruits. PsTIR1a, PsTIR1b, and PsAFB2 restored the auxin-sensitive root growth response to the mutant Arabidopsis seedlings Attir1-10 and/or Attir1-10 afb2-3. Expression of PsTIR1 or AtTIR1 in Attir1-10 afb2-3 mutants also restored the greater root inhibitory response of 4-Cl-IAA compared to that of IAA, implicating TIR1 receptors in this response. The ability of 4-Cl-IAA to stimulate a stronger DR5::GUS auxin response than IAA at the same concentration in pea pericarps was associated with its ability to enrich the auxin-receptor transcript pool with PsTIR1a and PsAFB2 by decreasing the transcript abundance of PsTIR1b (mimicking results in pericarps with developing seeds). Therefore, the markedly different effect of IAA and 4-Cl-IAA on pea fruit growth may at least partially involve TIR1/AFB receptors and the differential modulation of their population, resulting in specific Aux/IAA protein degradation that leads to an auxin-specific tissue response. |
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