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A dynamic pattern of local auxin sources is required for root regeneration

ABSTRACT: Following removal of its stem cell niche, the root meristem can regenerate by recruitment of remnant cells from the stump. Regeneration is initiated by rapid accumulation of auxin near the injury site but the source of this auxin is unknown. Here, we show that auxin accumulation arises from the activity of multiple auxin biosynthetic sources that are newly specified near the cut site and that their continuous activity is required for the regeneration process. Auxin synthesis is highly localized and PIN-mediate transport is dispensable for auxin accumulation and tip regeneration. Roots lacking the activity of the regeneration competence factor ERF115, or that are dissected at a zone of low-regeneration potential, fail to activate local auxin sources. Remarkably, restoring auxin supply is sufficient to confer regeneration capacity to these recalcitrant tissues. We suggest that regeneration competence relies on the ability to specify new local auxin sources in a precise spatio-temporal pattern.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE145488 | GEO | 2020/06/01

REPOSITORIES: GEO

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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 ERF115 expression synergistically drive stem cell regeneration

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

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A dynamic pattern of local auxin sources is required for root regeneration

Project description:A dynamic pattern of local auxin sources is required for root regeneration

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APC/CCCS52A2 repressed phytosulfokine signaling restricts root QC cell proliferation through ERF115 degradation

Project description:The quiescent center (QC) plays an essential role during root development by creating a microenvironment that preserves the stem cell fate of its surrounding cells. Strikingly, in order to retain root structure, QC cells only occasionally self-renew, displaying a proliferation rate far below that of all other cells within the root meristem. Previously, the APC/CCCS52A2 ubiquitine ligase and brassinosteroid signaling pathways have been found to antagonistically control Arabidopsis thaliana QC cell proliferation. Here, we demonstrate that both pathways converge on the ERF115 transcription factor that acts as a rate-limiting factor of QC cell division through transcriptional control of the autocrine phytosulfokine PSK5 peptide hormone. ERF115 marks QC cell division but is restrained through proteolysis by the APC/CCCS52A2 ubiquitine ligase, whereas QC proliferation is driven by brassinosteroid-dependent ERF115 expression. Combined, these two antagonistic mechanisms delimit the ERF115-PSK5 activity and QC renewal. Our results reveal a unique cell cycle regulatory mechanism that accounts for the low proliferation rate of QC cells within a surrounding population of highly mitotic active cells. ChIP-seq analysis of genes bound by the ERF115 transcription factor, using mock ChIP with wild type cells as negative control. Analyzed by Illumina HiSeq

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Transcript profiling of ERF115 transgenic Arabidopsis thaliana

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2013-11-04 | E-GEOD-48836 | biostudies-arrayexpress

PAT1-type GRAS-domain proteins control regeneration following wounding by transcriptional activation of DOF3.4 driving cell proliferation

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2023-04-26 | GSE200500 | GEO

Heat-induced cell damage induces autophagy-mediated cell expansion in Arabidopsis

Project description:Plants have evolved sophisticated cellular and molecular mechanisms to acclimate to adverse environmental stresses. Here, we report that acute heat stress induces excessive cell expansion, reaching up to 13,000 μm2, in Arabidopsis thaliana. The heat-induced cell expansion progressed along with programmed cell death. Autophagy was responsible for excessive cell expansion, as evidenced by autophagic structures in the expanded cells as well as failure of heat-induced cell expansion in autophagy-related 5-1 (atg5-1) and atg7-2 mutants. We also reveal that the transcription factor ETHYLENE RESPONSE FACTOR115 (ERF115), which is activated upon neighboring cell death, is involved in heat-induced cell expansion. ERF115 accumulation in response to heat possibly activated the expression of several ATGs by directly binding to gene promoters. In agreement, the erf115 phytochrome a signal transduction1-2 (pat1-2) double mutant exhibited reduced cell expansion under heat stress with diminished autophagic activity. Overall, our findings indicate that heat-stress-induced cell death triggers autophagy-mediated cell expansion in plant leaves, which may compensate for the death of nearby cells.

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