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Sanhueza, D.

Publications and source records attributed to Sanhueza, D..

2 recordsLinked to original sources

CSLB4-mediated cell wall remodeling decouples phloem access from aphid performance in Arabidopsis thaliana

The plant cell wall (CW) is a key determinant of plant defense; however, the extent to which natural variation in CW architecture contributes to resistance against phloem-feeding insects remains unclear. Here, we combined genome-wide association studies (GWAS) with functional analyses to identify genetic determinants of resistance against the specialist aphid Brevicoryne brassicae in Arabidopsis thaliana. GWAS conducted on 200 natural accessions identified a single locus on chromosome 2 associated with aphid performance. Integration of haplotype and epidermis-specific expression data prioritized CSLB4, a member of the cellulose synthase-like B family. Loss-of-function cslb4 mutants showed reduced aphid offspring, indicating enhanced resistance to B. brassicae, whereas performance of the generalist aphid Myzus persicae was unaffected. Electrical penetration graph analyses revealed earlier phloem access on cslb4 mutants despite reduced performance, indicating a decoupling between phloem access and aphid success. Biochemical and immunolocalization analyses showed that CSLB4 disruption altered CW architecture, including increased xyloglucan epitope accessibility in mesophyll cell walls and reduced callose deposition upon aphid infestation. In addition, CSLB4 localized to Golgi-associated compartments, and in silico analyses are consistent with a role in non-cellulosic polysaccharide biosynthesis. Together, these findings identified CSLB4 as a modulator of CW architecture that uncouples phloem access from aphid performance. HighlightA GWAS identifies CSLB4 as a regulator of cell wall architecture that uncouples aphid-feeding from performance, revealing a new mechanism of plant resistance to specialist insects.

plant biology↗

Transcriptomic reprogramming in a susceptible Phaseolus vulgaris L. variety during Pseudomonas syringae attack: The key role of homogalacturonan methylation

The susceptibility of common bean varieties to Pseudomonas syringae pv. phaseolicola (Pph) has been well-documented. However, the molecular mechanism that drives this susceptibility has not been clarified yet. In an attempt to understand this process, 15-day-old common bean plants, variety rinon, were infected with Pph to analyze the transcriptomic changes during the first steps of the infection (at 2 and 9 h). RNA-seq analysis showed an upregulation of defense-and signaling-related genes at 2h, most of them being downregulated at 9h, suggesting that Pph would inhibit the transcriptomic reprogramming of the plant. This trend was also observed in the modulation of 101 cell wall (CW) related genes, suggesting that Pph could produce/induce changes in the CW. However, the changes in CW composition at early stages of Pph infection were related to homogalacturonan (HG) methylation and the formation of HG egg boxes. From all HG-related genes modulated by the infection, a common bean pectin methylesterase inhibitor 3 (PvPMEI3) gene - closely related to AtPMEI3 -- was detected. In addition, PMEI3 protein was located in the apoplast and its PME inhibitory activity was demonstrated. Therefore, PvPMEI3 seems to be a good candidate to play a key role in Pph infection. This premise was supported by the analysis of Arabidopsis pmei3 mutant, which showed susceptibility to Pph, in contrast to resistant Col-0 control plants. All these changes could be an attempt to reinforce the CW structure and thus, hinder the attack of the bacterium. However, these transcriptional and CW-remodeling processes are neither maintained during the necessary time, nor are deep enough to block the action of the pathogen, facilitating the well-known susceptibility of rinon variety to Pph.

plant biology↗