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Arabidopsis transcription factor TCP13 promotes shade avoidance syndrome-like responses by directly targeting a subset of shade-responsive gene promoters

Authors
Hur, Yoon-SunOh, JeonghwaKim, NamukKim, SunghanSon, OraKim, JiyoungUm, Ji-HyunJi, ZuoweiKim, Min-haKo, Jae-HeungOhme-Takagi, MasaruChoi, GiltsuCheon, Choong-Ill
Issue Date
Jan-2024
Publisher
OXFORD UNIV PRESS
Keywords
Flavonoid biosynthesis; hypocotyl elongation; light signaling; phytochrome interacting factor 4 (PIF4); promoter targeting; shade avoidance syndrome; small auxin up RNA (SAUR); TCP13; transcriptional regulation
Citation
JOURNAL OF EXPERIMENTAL BOTANY, v.75, no.1, pp 241 - 257
Pages
17
Journal Title
JOURNAL OF EXPERIMENTAL BOTANY
Volume
75
Number
1
Start Page
241
End Page
257
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/159739
DOI
10.1093/jxb/erad402
ISSN
0022-0957
1460-2431
Abstract
TCP13 belongs to a subgroup of TCP transcription factors implicated in the shade avoidance syndrome (SAS), but its exact role remains unclear. Here, we show that 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 PHYTOCHROME-INTERACTING FACTOR (PIF)-auxin signaling in plants, but we found no evidence in a transcriptome analysis that TCP13 activates PIF-auxin signaling. Instead, TCP13 mimics shade by activating the expression of a subset of shade-inducible and cell elongation-promoting SAUR genes including SAUR19, by direct targeting of their promoters. We also found that 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 that TCP13 promotes the SAS-like response by directly targeting a subset of shade-responsive genes without activating the PIF-auxin signaling pathway. The Arabidopsis transcription factor TCP13 promotes shade avoidance syndrome-like responses by directly targeting a subset of shade-responsive gene promoters without activating the PIF-auxin signaling pathway.
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