TCP13 promotes shade avoidance syndrome-like responses by directly targeting a subset of shade-responsive gene promoters.
Yoon-Sun HurJeonghwa OhNamuk KimSunghan KimOra SonJiyoung KimJi-Hyun UmZuowei JiMin-Ha KimJae-Heung KoMasaru Ohme-TakagiGiltsu ChoiChoong-Ill CheonPublished in: Journal of experimental botany (2023)
TCP13 belongs to a TCP subgroup implicated in the shade avoidance syndrome (SAS), but its exact role remains unclear. Here, we show TCP13 promotes the SAS-like response by enhancing hypocotyl elongation and suppressing flavonoid biosynthesis as a part of the incoherent feed-forward loop in light signaling. Shade is known to promote the SAS by activating PIF-auxin signaling in plants, but we found no evidence in a transcriptome analysis that TCP13 activates PIF-auxin signaling. Instead, we found TCP13 mimics shade by activating the expression of a subset of shade-inducible and cell elongation-promoting SAUR genes including SAUR19, via direct targeting of their promoters. We also found TCP13 and PIF4, a molecular proxy for shade, repress the expression of flavonoid biosynthetic genes by directly targeting both shared and distinct sets of biosynthetic gene promoters. Together, our results indicate TCP13 promotes the SAS-like response by directly targeting a subset of shade-responsive genes without activating the PIF-auxin signaling pathway.
Keyphrases
- signaling pathway
- cancer therapy
- genome wide
- genome wide identification
- poor prognosis
- pi k akt
- dna methylation
- genome wide analysis
- transcription factor
- single cell
- epithelial mesenchymal transition
- gene expression
- bioinformatics analysis
- induced apoptosis
- mesenchymal stem cells
- cell therapy
- magnetic resonance
- oxidative stress
- bone marrow
- cell proliferation
- open label