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Rocks in the Auxin Stream: Wound induced auxin accumulation and ERF115 expression synergistically drive stem cell regeneration

ABSTRACT: Rocks in the Auxin Stream: Wound induced auxin accumulation and ERF115 expression synergistically drive stem cell regeneration

PROVIDER: PRJNA587008 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10382303.fastq.gz	Fastqsanger.gz
	SRR10382304.fastq.gz	Fastqsanger.gz
	SRR10382305.fastq.gz	Fastqsanger.gz
	SRR10382306.fastq.gz	Fastqsanger.gz
	SRR10382307.fastq.gz	Fastqsanger.gz

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Rocks in the Auxin Stream: Wound induced auxin accumulation and ERF115 expression synergistically drive stem cell regeneration

Project description:Plants are known for their outstanding capacity for recovering from various wounds and injury. However, it remains largely unknown how plants sense diverse forms of injury and canalize existing developmental processes into the execution of a correct regenerative response. Auxin, a cardinal plant hormone with morphogenlike properties, has been previously implicated in recovery from diverse types of wounding and organ loss. Here, through a combination of cellular imaging and in silico modelling, we demonstrate that vascular stem cell death obstructs the polar auxin flux, much alike rocks in a stream, and causes it to accumulate in the endodermis. This in turn grants the endodermal cells the capacity to undergo periclinal cell division that repopulate the vascular stem cell pool. Replenishment of the vasculature by the endodermis depends on the transcription factor ERF115, a wound inducible regulator of stem cell divisions. Although not being the primary inducer, auxin is required to maintain ERF115 expression. Reversely, ERF115 sensitizes cells to auxin by activating ARF5/MONOPTEROS, an auxin responsive transcription factor involved in the global auxin response, tissue patterning and organ formation. Combined, the wound induced auxin accumulation and ERF115 expression grant the endodermal cells stem cell activity. Our work provides a mechanistic model for wound induced stem cell regeneration in which ERF115 acts as a wound-inducible stem cell organizer that interprets wound-induced auxin maxima.

2020-06-30 | GSE139715 | GEO

Rocks in the auxin stream: Wound-induced auxin accumulation and <i>ERF115</i> expression synergistically drive stem cell regeneration.

Project description:Plants are known for their outstanding capacity to recover from various wounds and injuries. However, it remains largely unknown how plants sense diverse forms of injury and canalize existing developmental processes into the execution of a correct regenerative response. Auxin, a cardinal plant hormone with morphogen-like properties, has been previously implicated in the recovery from diverse types of wounding and organ loss. Here, through a combination of cellular imaging and in silico modeling, we demonstrate that vascular stem cell death obstructs the polar auxin flux, much alike rocks in a stream, and causes it to accumulate in the endodermis. This in turn grants the endodermal cells the capacity to undergo periclinal cell division to repopulate the vascular stem cell pool. Replenishment of the vasculature by the endodermis depends on the transcription factor ERF115, a wound-inducible regulator of stem cell division. Although not the primary inducer, auxin is required to maintain ERF115 expression. Conversely, ERF115 sensitizes cells to auxin by activating ARF5/MONOPTEROS, an auxin-responsive transcription factor involved in the global auxin response, tissue patterning, and organ formation. Together, the wound-induced auxin accumulation and ERF115 expression grant the endodermal cells stem cell activity. Our work provides a mechanistic model for wound-induced stem cell regeneration in which ERF115 acts as a wound-inducible stem cell organizer that interprets wound-induced auxin maxima.

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Interactions of ARF6 with PIF4, BZR1, and RGA integrate auxin signaling with environmental and other hormonal signals in Arabidopsis [ChIP-Seq]

Project description:Auxin is a major plant hormone for both development and environmental adaptation. Auxin responses are context dependent and highly modulated by light, temperature, the circadian clock, brassinosteroid, and gibberellin, but the underlying mechanisms remain unclear. Here, we show that auxin signaling integrates with other signals through direct interactions of AUXIN RESPONSE FACTOR6 (ARF6) with PHYTOCHROME INTERACTING FACTOR4 (PIF4), the brassinosteroid-signaling transcription factor BZR1, and the gibberellin-signaling repressor RGA. ChIP-Seq and RNA-Seq experiments show that ARF6, PIF4, and BZR1 bind to largely overlapping targets in the genome and synergistically activate gene expression. In vitro and in vivo assays show that ARF6-promoter binding is enhanced by PIF4 and BZR1 but blocked by RGA. Furthermore, a tripartite HLH/bHLH module feedback regulates PIF activity and thus modulates auxin sensitivity according to additional developmental and environmental cues. Our results demonstrate a central growth-regulation transcriptional network that coordinates hormonal, environmental, and developmental control of cell elongation and plant growth. Genome-wide identification of ARF6 DNA-binding sites in etiolated Arabidopsis seedlings.

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