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AT-hook transcription factors repress petiole growth by antagonizing PIF4 [RNA-seq]

ABSTRACT: As sessile organisms, plants rely heavily on growth and developmental plasticity to respond to external challenges threatening their survival. Strict regulation of growth in organs such as hypocotyls and petioles enables plants to respond optimally to varying environmental conditions, such as changes in light and temperature, while also ensuring that resources are not needlessly wasted on unnecessary growth. Studies performed in Arabidopsis thaliana have established the PHYTOCHROME INTERACTING FACTOR (PIF) transcription factor family as key positive regulators of growth, particularly in hypocotyls and petioles. In this study, we identify members of the AT-HOOK MOTIF NUCLEAR LOCALIZED (AHL) family, including SUPPRESSOR OF PHYTOCHROME B4-#3 (SOB3), as repressors of PIF4-mediated petiole elongation. Specifically, we found that high levels of SOB3 lead to a short-petiole phenotype similar to that conferred by removal of PIF4. Conversely, the dominant-negative sob3-6 mutant has long petioles, a phenotype which is dependent on PIF4. Additionally, we show that AHLs repress the expression of many PIF-activated genes, including a number involved in hormone-mediated promotion of growth and a subset of which are directly bound by both SOB3 and PIFs. Taken together these results suggest that AHLs repress petiole growth by antagonizing PIF-mediated transcriptional activation of growth-promoting genes, including ARABIDOPSIS THALIANA HOMEOBOX PROTEIN 2 (ATHB2), BRASSINOSTEROID INSENSITIVE 1 (BRI1), INDOLE-3-ACETIC ACID INDUCIBLE 19 (IAA19), PIN-FORMED 3 (PIN3), SMALL AUXIN UP RNA 24 (SAUR24), and YUCCA8 (YUC8). Elucidating a mechanism by which positive and negative growth factors influence growth in petioles achieves a critical first step towards understanding the gene regulatory networks which modulate leaf growth in response to the environment.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE122454 | GEO | 2020/03/19

REPOSITORIES: GEO

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Project description:Plants grown under a canopy recognize changes in light quality and modify their growth patterns; this modification is known as shade avoidance syndrome. In leaves, leaf blade expansion is suppressed, whereas petiole elongation is promoted under the shade. However, the mechanisms that control these responses are largely unclear. Here, we demonstrated that both auxin and brassinosteroid (BR) are required for the normal leaf responses to shade. The microarray analysis of leaf blades and petioles treated with end-of-day far-red light (EODFR) revealed that almost half of the genes induced by the treatment in both parts were previously identified as auxin-responsive genes. Likewise, BR-responsive genes were overrepresented in the EODFR-induced genes. Hence, the auxin and BR responses were elevated by EODFR treatment in both leaf blades and petioles, although opposing growth responses were observed in these two parts. The analysis of the auxin-deficient doc1/big mutant and BR-deficient rot3/cyp90c1 mutant further indicates that auxin and BR were equally required for the normal petiole elongation response to the shade stimulus. In addition, the spotlight irradiation experiment revealed that phytochrome in leaf blades but not that in petioles regulated petiole elongation, which was probably mediated through regulation of the auxin/BR responses in petioles. On the basis of these findings, we conclude that auxin and BR cooperatively promote petiole elongation in response to the shade stimulus under the control of phytochrome in the leaf blade. The WT seedlings were grown for 19 days under continuous white light condition before experimental treatment with three light conditions. Seedlings were either maintained in white light for 2 h (WL), incubated in the dark condition for 2 h (D), or experienced a pulse irradiation of FR light before incubated in the dark condition for 2 h (FRD). Total RNAs were separately prepared from leaf blades and petioles after each light treatment. Three independent biological replicates were used.

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AT-hook transcription factors repress petiole growth by antagonizing PIF4 [RNA-seq]

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