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Urquidi-Camacho, R. A.

Publications and source records attributed to Urquidi-Camacho, R. A..

3 recordsLinked to original sources

An updated model of shoot apical meristem regulation by ERECTA family and CLAVATA3 signaling pathways

The shoot apical meristem (SAM) gives rise to above-ground organs. The size of the SAM is relatively constant due to the balance of stem cell replenishment versus cell recruitment into developing organs. In angiosperms, the transcription factor WUSCHEL (WUS) promotes stem cell identity in the central zone of the SAM. WUS forms a negative feedback loop with a signaling pathway activated by CLAVATA3 (CLV3). In the periphery of the SAM, the ERECTA family (ERf) receptors promote cell differentiation and constrain the expression of WUS and CLV3. Here, we show that four ligands of ERfs redundantly inhibit CLV3 and WUS expression. Transcriptome analysis confirmed that WUS and CLV3 are the main targets of ERf signaling and uncovered several new ones. Analysis of promoter reporters indicated that in the vegetative meristem, the WUS expression domain mostly overlapped with the CLV3 domain and did not shift along the apical-basal axis in clv3. A 3D mathematical model reproduced the experimentally observed CLV3 and WUS expression patterns with fewer assumptions than earlier models. Based on these findings, we propose that CLV3 regulates cellular levels of WUS expression through autocrine signaling, while ERfs regulate WUS spatial expression, preventing its encroachment into the peripheral zone. One Sentence SummaryThrough autocrine signaling, CLV3 regulates the level of WUS expression in the vegetative SAM but not its location, while ERfs regulate the WUS spatial pattern, preventing its expansion into the peripheral zone.

plant biology↗

Initiation of aboveground organ primordia depends on combined action of auxin, ERECTA family genes, and PINOID.

Leaves and flowers are produced by the shoot apical meristem (SAM) at a certain distance from its center, a process that requires the hormone auxin. The amount of auxin and the pattern of its distribution in the initiation zone determine the size and spatial arrangement of organ primordia. Auxin gradients in the SAM are formed by PIN-FORMED (PIN) auxin efflux carriers whose polar localization in the plasma membrane depends on the protein kinase PINOID (PID). Previous work determined that ERECTA family genes (ERfs) control initiation of leaves. ERfs are plasma membrane receptors that enable cell-to-cell communications by sensing extracellular small proteins from Epidermal Patterning Factor/EPF-like (EPF/EPFL) family. Here, we investigate whether ERfs regulate initiation of organs by altering auxin distribution or signaling. Genetic and pharmacological data suggest that ERfs do not regulate organogenesis through PINs while transcriptomics data show ERfs do not alter primary transcriptional responses to auxin. Our results indicate that in the absence of ERf signaling, the peripheral zone cells inefficiently initiate leaves in response to auxin signals and that increased accumulation of auxin in the er erl1 erl2 SAM can partially rescue organ initiation defects. We propose that both auxin and ERfs are essential for leaf initiation, and that they have common downstream targets. Genetic data also indicate that the role of PID in initiation of cotyledons and leaves cannot be attributed solely to regulation of PIN polarity, and PID is likely to have other functions in addition to regulation of auxin distribution. Summary statementAuxin is unable to promote cotyledon and leaf initiation in the absence of signaling by ERECTA family receptor kinases and the kinase PINOID.

plant biology↗

Light activates the translational regulatory GCN2 kinase via reactive oxygen species emanating from the chloroplast

Cytosolic mRNA translation is subject to global and mRNA-specific controls. Phosphorylation of translation initiation factor eIF2 anchors a reversible switch that represses translation globally. The stress-responsive GCN2 kinase is the only known kinase for eIF2 in Arabidopsis. Here we show that conditions that generate reactive oxygen species (ROS) in the chloroplast, such as dark-light transitions, high light, and the herbicide methyl viologen all rapidly activated the GCN2 kinase, whereas mitochondrial and ER stress did not. In addition, GCN2 activation was light dependent and mitigated by photosynthesis inhibitors and ROS quenchers. Accordingly, seedling growth of multiple gcn2 mutant alleles was retarded under conditions of excess light, implicating the GCN2-eIF2 pathway in responses to light and associated ROS. Once activated, the GCN2 kinase preferentially suppressed the ribosome loading of mRNAs for functions such as mitochondrial ATP synthesis, the chloroplast thylakoids, vesicle trafficking, and translation. The transcriptome of gcn2 mutants was sensitized to abiotic stress, including oxidative stress, as well as innate immune responses. Accordingly, gcn2 displayed defects in immune priming by the fungal elicitor, chitin. In conclusion, we provide evidence that reactive oxygen species produced by the photosynthetic apparatus help to activate the highly conserved GCN2 kinase, leading to eIF2 phosphorylation and thus affecting the status of the cytosolic protein synthesis apparatus.

plant biology↗