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Blanco-Herrera, F.

Publications and source records attributed to Blanco-Herrera, F..

4 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↗

Salicylic acid contributes to plant defense against a necrotroph: evidence from a transgenic NahG-expressing strain in Botrytis cinerea.

Botrytis cinerea is a plant pathogen that causes significant agricultural losses worldwide. Although this necrotroph disrupts extensive plant hormonal networks, the role of salicylic acid (SA) in plant defense against B. cinerea remains controversial across plant species. To investigate its role from a pathogen perspective, B. cinerea mutants constitutively expressing the Pseudomonas putida salicylate hydroxylase NahG, an enzyme that catalyzes salicylic acid degradation, were generated. The NahG-expressing B. cinerea mutants exhibited enhanced in vitro growth on SA-supplemented media, indicating that SA catabolism confers an advantage. In planta, these mutants displayed increased virulence in Arabidopsis thaliana and Phaseolus vulgaris. Notably, the increase in lesion formation was strictly dependent on host SA biosynthesis, as no differences were observed when infecting the SA-deficient Arabidopsis sid2-2 mutant. This result provides evidence that SA degradation increases the virulence of B. cinerea in the interaction with A. thaliana. Genome inspection revealed that the fungus encodes four salicylate hydroxylase-like genes. Analysis of publicly available transcriptomic data from virulence assays across multiple plant hosts revealed that all these genes are expressed during the plant-pathogen interaction, with distinct expression patterns across infection stages and hosts. Together, these observations suggest that B. cinerea may have endogenous mechanisms for SA degradation during host colonization, thereby conferring the capacity to control its accumulation during the infection process. HIGHLIGHTSO_LIBotrytis cinerea expressing the salicylate hydroxylase (SH) ppNahG shows enhanced virulence in Arabidopsis and bean plants. C_LIO_LIEnhanced virulence of NahG-expressing strains depends on host salicylic acid biosynthesis. C_LIO_LIThe Botrytis cinerea genome encodes four SH-like genes. C_LIO_LISH-like genes display distinct expression patterns during infection across different plant hosts. C_LI VISUAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=128 SRC="FIGDIR/small/698134v1_ufig1.gif" ALT="Figure 1"> View larger version (24K): org.highwire.dtl.DTLVardef@135adorg.highwire.dtl.DTLVardef@16b2947org.highwire.dtl.DTLVardef@62fd40org.highwire.dtl.DTLVardef@e07e2e_HPS_FORMAT_FIGEXP M_FIG C_FIG

plant biology↗

The Arabidopsis TNL immune receptor BNT1 localizes to the plastid envelope and mediates flg22-induced resistance against Pseudomonas

Precise localization and trafficking of plant immune receptors are critical for their function. We identify the TNL-class nucleotide-binding leucine-rich repeat receptor (NLR) BURNOUT1 (BNT1) from Arabidopsis thaliana as localized to plastids, key organelles for plant immunity. Alternative transcription start site usage generates two isoforms of BNT1: BNT1.2, which is targeted to the plastid envelope via an N-terminal signal-anchored mechanism, and BNT1.1, which resides in the cytoplasm. Moreover, BNT1.2 is predominantly expressed in epidermal cells, where it localizes to the so-called sensory plastids. Functional analysis revealed that bnt1 mutants exhibit compromised PAMP-triggered immunity (PTI) responses, including impaired callose deposition and reduced flg22-induced resistance to Pseudomonas syringae pv. tomato, while flg22-induced apoplastic reactive oxygen species production remains unaffected. Notably, only the plastid-localized BNT1.2 isoform is required for these PTI responses. Our findings reveal a role for NLRs in regulating PTI responses from plastids and highlight these organelles as key hubs for signal(s) integration during plant-pathogen interactions. Significance statementThis study identifies BNT1 as a TNL-class immune receptor localized to the plastid envelope. Two distinct isoforms of BNT1 were characterized: one with a plastid-targeting signal anchor that ensures plastid localization and another confined to the cytoplasm. Notably, only the plastid-localized isoform mediates PTI responses and confers resistance to Pseudomonas, highlighting the critical role of precise NLR localization and the central role of plastids in plant immunity.

plant biology↗

Photosynthetic and Genetic Adaptations Underpinning the Resilience of Cistanthe longiscapa in the Atacama Desert

O_LIThe Atacama Desert is one of the most hostile environments for life. However, the plant species Cistanthe longiscapa (C. longiscapa) completes its life cycle in the Atacama Desert after sporadic rainfall. C_LIO_LIPhysiological analyses under controlled environmental conditions revealed superior photosynthetic performance, better light acclimation mechanisms, and larger accumulation of photosystem II in C. longiscapa compared to its mesophilic sister species. C_LIO_LIC. longiscapa shows evolutionary expansions in gene families related to DNA repair, photosynthesis, and protein homeostasis. In addition, we observed substantial gene duplication and polymorphic variations between coastal and inland populations in the Atacama Desert. Finally, our assembled mitochondrial genome provides genetic information for all DNA-containing compartments of C. longiscapa. C_LIO_LIDiurnal oscillations of malic acid and time-resolved transcriptome analyses of plants harvested in the Atacama Desert indicate that C. longiscapa engages in CAM metabolism. We observed significant differences in transcripts encoding plastid-localized proteins, including those involved in carbon metabolism, light harvesting, and photoprotection, highlighting the critical role of chloroplasts in the adaptation of C. longiscapa to the Atacama Desert. C_LIO_LIOur study provides physiological and genetic evidence for the adaptations of C. longiscapa and advances our understanding of how plants can cope with extreme environmental conditions. C_LI

plant biology↗