Hormonal regulation of the BRC1-dependent strigolactone transcriptome involved in shoot branching responses
Kerr, S. C.; de Saint Germain, A.; Dissanayake, I. M.; Mason, M. G.; Dun, E. A.; Tanurdzic, M.; Beveridge, C. A.
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The plant hormone strigolactone (SL) inhibits shoot branching by suppressing the growth of axillary buds. This is thought to occur largely via regulation of the transcription factor BRANCHED1 (BRC1). Here, we clarify the central role of BRC1 and identify additional transcriptional responses by which SL might regulate axillary bud outgrowth in garden pea (Pisum sativum). We used a transcriptomic approach to identify differentially expressed transcripts in pea axillary buds in response to a synthetic SL, rac-GR24. Changes in transcript abundance were confirmed by measuring their response to GR245DS. BRC1 was required for the regulation of over half of the fourteen GR245DS-regulated genes, confirming its role as a mediator of SL transcriptional responses in axillary buds. All, but one, of the BRC1-dependent GR245DS-regulated genes were also regulated by branch-promoting treatments cytokinin (CK) and/or decapitation in an opposing manner to SL. This suggests that SL, CK, and decapitation regulate shoot branching via a common pathway. We used correlational analyses of gene co-expression data to infer a gene regulatory network consisting of nine key co-expression modules correlated with rac-GR24 treatment. Enrichment of GO terms such as cell proliferation, carbohydrate responses, and abscisic acid and jasmonic acid hormone pathways suggest a role for these in SL-mediated inhibition of shoot branching. In summary, we have shown that BRC1 is indeed a key transcriptional regulator of the SL signalling pathway in pea buds as well as a focal point of the SL, CK and decapitation signalling pathways to coordinate shoot branching in pea buds. One Sentence SummaryIdentification of genes that are strigolactone-responsive and BRC1-dependent in pea buds reveals a high degree of overlap among strigolactone, cytokinin and decapitation response pathways.
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