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is a novel allele of present in the T-DNA line SALK_015201. | LitMetric

AI Article Synopsis

Article Abstract

Auxin is a hormone that is required for hypocotyl elongation during seedling development. In response to auxin, rapid changes in transcript and protein abundance occur in hypocotyls, and some auxin responsive gene expression is linked to hypocotyl growth. To functionally validate proteomic studies, a reverse genetics screen was performed on mutants in auxin-regulated proteins to identify novel regulators of plant growth. This uncovered a long hypocotyl mutant, which we called , in an annotated insertion line in (). Overexpression of the gene failed to rescue the phenotype and characterization of a second T-DNA allele of IRR found that it had a wild-type (WT) hypocotyl length. The mutant has an elevated expression of numerous genes associated with the brassinosteroid-auxin-phytochrome (BAP) regulatory module compared to WT, including transcription factors that regulate brassinosteroid, auxin, and phytochrome pathways. Additionally, seedlings fail to exhibit a strong transcriptional response to auxin. Using whole genome sequence data and genetic complementation analysis with SALK_015201C, we determined that a novel single nucleotide polymorphism in was responsible for the phenotype. This is predicted to induce a frameshift and premature stop codon at leucine 1125, within the histidine kinase-related domain of the carboxy terminus of PHYB, which is required for phytochrome signaling and function. Genetic complementation analyses with confirmed that is a mutant allele of . This study advances our understanding of the molecular mechanisms in seedling development, by furthering our understanding of how light signaling is linked to auxin-dependent cell elongation. Furthermore, this study highlights the importance of confirming the genetic identity of research material before attributing phenotypes to known mutations sourced from T-DNA stocks.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8197431PMC
http://dx.doi.org/10.1002/pld3.326DOI Listing

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