Biology subjects

Herrera-Vasquez, A.

Publications and source records attributed to Herrera-Vasquez, A..

5 recordsLinked to original sources

bioRxiv2026

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↗

bioRxiv2026

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↗

bioRxiv2025

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↗

bioRxiv2020

GSTU7 affects growth performance and acts as an antagonist of oxidative stress induced by methyl viologen

Plant glutathione S-transferases (GSTs) are glutathione-dependent enzymes with versatile functions, mainly related to detoxification of electrophilic xenobiotics and peroxides. The Arabidopsis genome codes for 53 GSTs, divided into seven subclasses, however understanding of their precise functions is limited. A recent study showed that class II TGA transcription factors TGA2, TGA5 and TGA6 are essential for tolerance of UV-B-induced oxidative stress and that this tolerance is associated with an antioxidative function of cytosolic tau-class GSTUs. Specifically, TGA2 controls the expression of several GSTUs under UV-B light and constitutive expression of GSTU7 in the tga256 triple mutant is sufficient to revert the UV-B-susceptible phenotype of tga256. To further study the function of GSTU7, we characterized its role in mitigation of oxidative damage caused by the herbicide methyl viologen (MV). Under non-stress conditions, gstu7 null mutants were smaller than wild-type (WT) plants and delayed in the onset of the MV-induced antioxidative response, which led to accumulation of hydrogen peroxide and diminished seedling survival. Complementation of gstu7 by constitutively expressed GSTU7 rescued these phenotypes. Furthermore, live monitoring of the glutathione redox potential in intact cells with the fluorescent probe Grx1-roGFP2 revealed that GSTU7 overexpression completely abolished the MV-induced oxidation of the cytosolic glutathione buffer compared to WT plants. GSTU7 was found to act as a glutathione peroxidase able to complement the lack of peroxidase-type GSTs in yeast. Together, these findings show that GSTU7 is crucial in the antioxidative response by limiting oxidative damage and thus protecting cells from oxidative stress.

plant biology↗

bioRxiv2020

Transcription factor TGA2 is essential for UV-B stress tolerance controlling oxidative stress in Arabidopsis

Plants possess a diversity of Reactive Oxygen Species (ROS)-processing enzymes involved in sensing and controlling ROS levels under basal and stressful conditions. There is little information on the transcriptional regulators that control the expression of these ROS-processing enzymes, particularly at the onset of the defense response to abiotic stress. Filling this gap, this paper reports a critical role for Arabidopsis TGA class II factors (TGA2, TGA5, and TGA6) in the tolerance response to UV-B light and photooxidative stress, by activating the expression of genes with antioxidative roles. We identified two clusters of genes responsive to UV-B and activated by TGA2/5/6 were identified using RNAseq and clustering analysis. The GSTU gene family, which encodes glutathione transferase enzymes from the Tau subclass, was overrepresented in these clusters. We corroborated the TGA2-mediated activation in response to UV-B for three model genes (GSTU7, GSTU8, and GSTU25) using RT-qPCR and ChIP analyses. Interestingly, using tga256 mutant and TGA2- and GSTU7-complemented mutant plants, we demonstrated that TGA2-mediated induction of GSTU genes is essential to control ROS levels and oxidative damage after UV-B and MeV treatments. This evidence positions TGA class II factors, particularly TGA2, as a key players in the redox signaling network of Arabidopsis plants. HighlightArabidopsis TGA2 transcription factor is part of the redox-signaling network controlling ROS levels and oxidative damage in tolerance response to UV-B and photooxidative stress, via activation of antioxidant GSTU genes.

plant biology↗