Forward genetic screen for auxin-deficient mutants by cytokinin
Jazyk angličtina Země Velká Británie, Anglie Médium electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
26143750
PubMed Central
PMC4491711
DOI
10.1038/srep11923
PII: srep11923
Knihovny.cz E-zdroje
- MeSH
- Arabidopsis enzymologie genetika MeSH
- biologický transport účinky léků MeSH
- cytokininy metabolismus MeSH
- fenotyp MeSH
- kořeny rostlin enzymologie genetika růst a vývoj MeSH
- kyseliny indoloctové metabolismus farmakologie MeSH
- mutace MeSH
- proteiny huseníčku genetika metabolismus MeSH
- regulátory růstu rostlin biosyntéza MeSH
- semenáček účinky léků růst a vývoj metabolismus MeSH
- signální transdukce účinky léků MeSH
- tryptofantransaminasa genetika metabolismus MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- cytokininy MeSH
- indoleacetic acid MeSH Prohlížeč
- kyseliny indoloctové MeSH
- proteiny huseníčku MeSH
- regulátory růstu rostlin MeSH
- tryptofantransaminasa MeSH
Identification of mutants with impairments in auxin biosynthesis and dynamics by forward genetic screening is hindered by the complexity, redundancy and necessity of the pathways involved. Furthermore, although a few auxin-deficient mutants have been recently identified by screening for altered responses to shade, ethylene, N-1-naphthylphthalamic acid (NPA) or cytokinin (CK), there is still a lack of robust markers for systematically isolating such mutants. We hypothesized that a potentially suitable phenotypic marker is root curling induced by CK, as observed in the auxin biosynthesis mutant CK-induced root curling 1 / tryptophan aminotransferase of Arabidopsis 1 (ckrc1/taa1). Phenotypic observations, genetic analyses and biochemical complementation tests of Arabidopsis seedlings displaying the trait in large-scale genetic screens showed that it can facilitate isolation of mutants with perturbations in auxin biosynthesis, transport and signaling. However, unlike transport/signaling mutants, the curled (or wavy) root phenotypes of auxin-deficient mutants were significantly induced by CKs and could be rescued by exogenous auxins. Mutants allelic to several known auxin biosynthesis mutants were re-isolated, but several new classes of auxin-deficient mutants were also isolated. The findings show that CK-induced root curling provides an effective marker for discovering genes involved in auxin biosynthesis or homeostasis.
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