Plant hormones (Literature sources on phytohormones and plant signalling)
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The hormonal, metabolic, and environmental regulation of plant shoot branching - Review

Authors: Yuqi Liu, Shangyu Chen, Sikander Pal, Jingquan Yu, Yanhong Zhou, Lam-Son Phan Tran and Xiaojian Xia. 

New Crops (2024)

Abstract: "Plants have evolved varied structures for environmental adaptation. Shoot branching, as a part of plant architecture, influences the allocation of sugars produced by photosynthesis and thus greatly impacts crop yields. The activity of axillary meristem, and apical dominance governs the shoot branching patterns. In this review, we summarize the key factors involved in the formation of lateral branches, and the mechanisms of how these factors are interconnected. In particular, we focus on recent advances in understanding how sugar and environmental signals affect the hormonal signaling network to regulate apical dominance. Ultimately, we propose that epigenetic modifications are critical mechanisms underlying the plasticity of shoot branching, and that precise targeted gene editing is promising for shaping the ideal plant architecture."
Julio Retamales's insight:
Good review!

Text of figure above: "Fig. 5. The environment regulation of bud activation. (A) The ratio of red and far-red light (R/FR) controls bud outgrowth. Phytochromes (PHYs) are the primary photoreceptors in this process. The high ratio of R/FR activates and stabilizes PHYB, suppressing auxin synthesis and signaling. PHYB-dependent light signaling also activates HY5. HY5 proteins in leaves translocate to buds and directly regulate the expression of BRC1 and bud growth. Meanwhile, PHYB regulates BRC1 expression through PIFs. FAR-RED ELONGATED HYPOCOTYLS 3 (FHY3) and FAR-RED IMPAIRED RESPONSE 1 (FAR1), two transcription factors essential for PHYA-mediated light signaling, suppress BRC1 expression by activating D53-like genes, or by suppressing the activity of SPL factors. (B) Nutrients in soil affect shoot branching through CK and SLs. Sufficient nitrogen and phosphate in the soil promote CK synthesis while suppressing the synthesis of SLs. Low levels of nitrogen and phosphate have the opposite effects on CK and SL synthesis. CK and SLs in roots moved to shoots to regulate lateral bud growth."
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The AGAMOUS-LIKE 16–GENERAL REGULATORY FACTOR 1 module regulates axillary bud outgrowth via catabolism of abscisic acid in cucumber

Authors: Jiacai Chen, Liu Liu, Guanghui Wang, Guangxin Chen, Xiaofeng Liu, Min Li, Lijie Han, Weiyuan Song, Shaoyun Wang, Chuang Li, Zhongyi Wang, Yuxiang Huang, Chaoheng Gu, Zhengan Yang, Zhaoyang Zhou, Jianyu Zhao and Xiaolan Zhang. 

The Plant Cell (2024)

One-sentence summary: CsAGL16 positively regulates axillary bud outgrowth in cucumber by directly promoting CsCYP707A4-mediated ABA catabolism, and CsGRF1 interacts with CsAGL16 and antagonizes the CsAGL16-mediated CsCYP707A4 activation.

Abstract: "Lateral branches are important components of shoot architecture and directly affect crop yield and production cost. Although sporadic studies have implicated abscisic acid (ABA) biosynthesis in axillary bud outgrowth, the function of ABA catabolism and its upstream regulators in shoot branching remain elusive. Here, we showed that the MADS-box transcription factor AGAMOUS-LIKE 16 (CsAGL16) is a positive regulator of axillary bud outgrowth in cucumber (Cucumis sativus). Functional disruption of CsAGL16 led to reduced bud outgrowth, whereas overexpression of CsAGL16 resulted in enhanced branching. CsAGL16 directly binds to the promoter of the ABA 8'-hydroxylase gene CsCYP707A4 and promotes its expression. Loss of CsCYP707A4 function inhibited axillary bud outgrowth and increased ABA levels. Elevated expression of CsCYP707A4 or treatment with an ABA biosynthesis inhibitor largely rescued the Csagl16 mutant phenotype. Moreover, cucumber General Regulatory Factor 1 (CsGRF1) interacts with CsAGL16 and antagonizes CsAGL16-mediated CsCYP707A4 activation. Disruption of CsGRF1 resulted in elongated branches and decreased ABA levels in the axillary buds. The Csagl16 Csgrf1 double mutant exhibited a branching phenotype resembling that of the Csagl16 single mutant. Therefore, our data suggest that the CsAGL16–CsGRF1 module regulates axillary bud outgrowth via CsCYP707A4-mediated ABA catabolism in cucumber. Our findings provide a strategy to manipulate ABA levels in axillary buds during crop breeding to produce desirable branching phenotypes."
Julio Retamales's insight:
Relevant finding!

Text of figure above: "Figure 10. The working model of CsAGL16-CsGRF1 regulates axillary bud outgrowth via CsCYP707A4-mediated ABA catabolism in cucumber. A) CsAGL16 directly binds to the promoter of CsCYP707A4 and activates its expression, resulted in elevated ABA catabolism and stimulation of axillary bud outgrowth. B) CsGRF1 can interact with CsAGL16 at the protein level, which inhibits the transcriptional activation of CsCYP707A4 by CsAGL16, leading to a reduction of catabolized ABA, increased ABA level in axillary buds and inhibition of lateral bud outgrowth. SAM, shoot apical meristem. ABA, abscisic acid. Arrow represents promotion. T-shaped represents inhibition."
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Ectopic expression of the apple cytokinin response regulator MdRR9 gene in tomatoes promotes shoot branching

Ectopic expression of the apple cytokinin response regulator MdRR9 gene in tomatoes promotes shoot branching | Plant hormones (Literature sources on phytohormones and plant signalling) | Scoop.it
Authors: Qian Zhao, Hao Chen, Dong Zhang and Juanjuan Ma. 

Scientia Horticulturae (2023)

Highlights • MdRR9 has an ORF of 648 bp, which showed the highest expression level in the stem and was up-regulated earlier in response to 6-BA than decapitation treatment. • The subcellular localization of MdRR9 was in the nucleus. Ectopic expression of MdRR9 in tomato indicated that MdRR9 plays a positive role in branch control. • Yeast double-hybrid assay showed that MdRR9 may interact with MADS-box transcription factor 22-like (AGL9). 

Abstract: "Response regulator 9 (RR9) is a typical member of type-A RRs whose transcription is rapidly increased by exogenous cytokinin (CTK). CTK stimulates the outgrowth of axillary buds in apples (Malus domestica). Previous studies showed that the decreased bud outgrowth activity of type-A rr mutants is paradoxical given that type-A RRs act as negative feedback regulators of CTK signaling in Arabidopsis. However, no systematic study of RR9 has been performed in apples. In this study, the genomic sequences of MdRR9, located on chromosome 14, were obtained. Sequencing identified MdRR9 as having an open reading frame (ORF) of 648 bp. Expression pattern showed MdRR9 has the highest expression level in the stem. MdRR9 was up-regulated earlier in response to 6-benzylaminopurine (6-BA, a synthetic type of CTK) than decapitation treatment. The subcellular localization of MdRR9 was in the nucleus. Ectopic expression of MdRR9 in tomatoes indicates that MdRR9 plays a positive role in branch control. A yeast double-hybrid assay showed that MdRR9 may interact with MADS-box transcription factor 22-like (MdAGL9), which gives us a new perspective to study the regulation of the bud outgrowth mechanism of RR9 in the future."
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PsmiR159b-PsMYB65 module functions in the resumption of bud growth after endodormancy by affecting the cell cycle in tree peony 

Authors: Tao Zhang, Xinyu Wang, Yanchao Yuan, Shoujie Zhu, Chunying Liu, Yuxi Zhang, Shupeng Gai.


Horticulture Research (2024)


Abstract: "Bud endodormancy in perennial plants is a sophisticated system that adapts to seasonal climatic changes. Growth-promoting signals such as low temperature and gibberellins (GAs) are crucial for facilitating budbreak following endodormancy release (EDR). However, the regulatory mechanisms underlying GA-mediated budbreak in tree peony (Paeonia suffruticosa) remain unclear. In tree peony, the expression of PsmiR159b among three differentially expressed miR159 members was inhibited with the prolonged chilling, and overexpression of PsMIR159b delayed budbreak, whereas silencing PsmiR159b promoted budbreak after dormancy. PsMYB65, a downstream transcription factor in the GA pathway, was induced by prolonged chilling and exogenous GA3 treatments. PsMYB65 was identified as a target of PsmiR159b, and promoted budbreak in tree peony. RNA-seq of PsMYB65-silenced buds revealed significant enrichment in the GO terms regulation of ‘cell cycle’ and ‘DNA replication’ among differentially expressed genes. Yeast one-hybrid and electrophoretic mobility shift assays demonstrated that PsMYB65 directly bound to the promoter of the type-D cyclin gene PsCYCD3;1. Dual-luciferase reporter assay indicated that PsMYB65 positively regulate PsCYCD3;1 expression, suggesting that miR159b-PsMYB65 module contributes to budbreak by influencing the cell cycle. Our findings revealed that the PsmiR159b-PsMYB65 module functioned in budbreak after dormancy by regulating cell proliferation, providing valuable insights into the endodormancy release regulation mechanism."

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Text of figure above: "PsmiR159b inhibited tree peony budbreak. (A) Morphology of PsMIR159b-overexpressing (OE-MIR159b) and PsMIR159b-silenced (STTM159b) buds. pCVA, transgenic buds with empty pCVA vector. Buds were pictured at 10 and 20 d after infection (DAI). Scale bar, 5 mm. (B) Relative level of PsmiR159b at 10 DAI. (C) Relative growth rate of OE-MIR159b and STTM159b buds at 10 and 20 DAI. (D) Expression levels of D-type cyclin (CYCDs) in OE-MIR159b, STTM159b buds and control at 10 DAI." 
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Transcription factor FveMYB117a inhibits axillary bud outgrowth by regulating cytokinin homeostasis in woodland strawberry

Authors: Yafan Han, Minghao Qu, Zhongchi Liu and Chunying Kang.


The Plant Cell (2024)


One-sentence summary: An MYB transcription factor directly regulates cytokinin homeostasis to repress axillary bud growth and consequently affect crown formation in woodland strawberry.


Abstract: "Shoot branching affects plant architecture. In strawberry (Fragaria L.), short branches (crowns) develop from dormant axillary buds to form inflorescences and flowers. While this developmental transition contributes greatly to perenniality and yield in strawberry, its regulatory mechanism remains unclear and understudied. In the woodland strawberry (Fragaria vesca), we identified and characterized two independent mutants showing more crowns. Both mutant alleles reside in FveMYB117a, a R2R3-MYB transcription factor gene highly expressed in shoot apical meristems, axillary buds and young leaves. Transcriptome analysis revealed that the expression of several cytokinin pathway genes was altered in the fvemyb117a mutant. Consistently, active cytokinins were significantly increased in the axillary buds of the fvemyb117a mutant. Exogenous application of cytokinin enhanced crown outgrowth in the wild type, whereas the cytokinin inhibitors suppressed crown outgrowth in the fvemyb117a mutant. FveMYB117a binds directly to the promoters of the cytokinin homeostasis genes FveIPT2 encoding an isopentenyltransferase and FveCKX1 encoding a cytokinin oxidase to regulate their expression. Conversely, the type-B Arabidopsis response regulators FveARR1 and FveARR2b can directly inhibit the expression of FveMYB117a, indicative of a negative feedback regulation. In conclusion, we identified FveMYB117a as a key repressor of crown outgrowth by inhibiting cytokinin accumulation and provide a mechanistic basis for bud fate transition in an herbaceous perennial plant."

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Relevant paper!

Text of the figure above: "Figure 9. A working model of FveMYB117a in crown outgrowth in woodland strawberry. In woodland strawberry, FveMYB117a is a key repressor of axillary bud outgrowth for crown formation. FveMYB117a directly regulates the expression of FveIPT2 and FveCKX1 to repress cytokinin (CK) accumulation. Other CK homeostasis genes that may be involved are not shown here. Conversely, FveARR1 and FveARR2b inhibit the expression of FveMYB117a to dampen its effect. In addition, FveMYB117a leads to higher levels of indole-3-acetic acid (IAA) and abscisic acid (ABA). FveBRC1 may be an integrator of these signals in regulating the bud transition from dormancy to outgrowth. Dotted lines are hypothetical and untested."
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Overexpression of SHORT-ROOT2 transcription factor enhanced the outgrowth of mature axillary buds in poplar trees

Overexpression of SHORT-ROOT2 transcription factor enhanced the outgrowth of mature axillary buds in poplar trees | Plant hormones (Literature sources on phytohormones and plant signalling) | Scoop.it
Authors: Minglei Yi, Heyu Yang, Shaohui Yang and Jiehua Wang.

Journal of Experimental Botany (2022)

Abstract: "SHORT-ROOT (SHR) transcription factors play important roles in asymmetric cell division and radial patterning of Arabidopsis root. In hybrid poplar (P. tremula × P. alba clone INRA 717-1B4), PtaSHR2 was preferentially expressed in axillary buds (AXBs) and transcriptionally upregulated during AXB maturation and activation. Overexpression of SHR2 (PtSHR2OE) induced an enhanced outgrowth of AXBs below the bud maturation point with a simultaneous transition of an active shoot apex into an arrested terminal bud. The larger and more mature AXBs of PtSHR2OE trees revealed altered expression levels of genes involved in axillary meristem initiation and bud activation as well as a higher ratio of cytokinin to auxin. With the aim to elucidate the underlying mechanism of PtSHR2OE-induced high branching, subsequent molecular and biochemical studies showed that compared to wild-type trees, decapitation induced a quicker bud outburst in PtSHR2OE trees, which could be fully inhibited by exogenous application of auxin or cytokinin biosynthesis inhibitor, but not by N-1-naphthylphthalamic acid. Our results indicated that overexpression of PtSHR2B disturbed the internal hormonal balance in AXBs by interfering with the basipetal transport of auxin, rather than causing auxin biosynthesis deficiency or auxin insensitivity, thereby releasing mature AXBs from the apical dominance and promoting their outgrowth."
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This article was already posted here when published as a preprint. 
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