Epigenetic differences between wild and cultivated grapevines highlight the contribution of DNA methylation during crop domestication.

The domestication process in grapevines has facilitated the fixation of desired traits. Nowadays, vegetative propagation through cuttings enables easier preservation of these genotypes compared to sexual reproduction. Nonetheless, even with vegetative propagation, various phenotypes are often present within the same vineyard due to the accumulation of somatic mutations. These mutations are not the sole factors influencing phenotype. Alongside somatic variations, epigenetic variation has been proposed as a pivotal player in regulating phenotypic variability acquired during domestication. The emergence of these epialleles might have significantly influenced grapevine domestication over time. This study aims to investigate the impact of domestication on methylation patterns in cultivated grapevines. Reduced-representation bisulfite sequencing was conducted on 18 cultivated and wild accessions. Results revealed that cultivated grapevines exhibited higher methylation levels than their wild counterparts. Differential Methylation Analysis between wild and cultivated grapevines identified a total of 9955 differentially methylated cytosines, of which 78% were hypermethylated in cultivated grapevines. Functional analysis shows that core methylated genes (consistently methylated in both wild and cultivated accessions) are associated with stress response and terpenoid/isoprenoid metabolic processes. Meanwhile, genes with differential methylation are linked to protein targeting to the peroxisome, ethylene regulation, histone modifications, and defense response. Collectively, our results highlight the significant roles that epialleles may have played throughout the domestication history of grapevines.

WRKY6 transcription factor restricts arsenate uptake and transposon activation in Arabidopsis.

Stress constantly challenges plant adaptation to the environment. Of all stress types, arsenic was a major threat during the early evolution of plants. The most prevalent chemical form of arsenic is arsenate, whose similarity to phosphate renders it easily incorporated into cells via the phosphate transporters. Here, we found that arsenate stress provokes a notable transposon burst in plants, in coordination with arsenate/phosphate transporter repression, which immediately restricts arsenate uptake. This repression was accompanied by delocalization of the phosphate transporter from the plasma membrane. When arsenate was removed, the system rapidly restored transcriptional expression and membrane localization of the transporter. We identify WRKY6 as an arsenate-responsive transcription factor that mediates arsenate/phosphate transporter gene expression and restricts arsenate-induced transposon activation. Plants therefore have a dual WRKY-dependent signaling mechanism that modulates arsenate uptake and transposon expression, providing a coordinated strategy for arsenate tolerance and transposon gene silencing.

Role of actin cytoskeleton in brassinosteroid signaling and in its integration with the auxin response in plants.

In plants, developmental programs and tropisms are modulated by the phytohormone auxin. Auxin reconfigures the actin cytoskeleton, which controls polar localization of auxin transporters such as PIN2 and thus determines cell-type-specific responses. In conjunction with a second growth-promoting phytohormone, brassinosteroid (BR), auxin synergistically enhances growth and gene transcription. We show that BR alters actin configuration and PIN2 localization in a manner similar to that of auxin. We describe a BR constitutive-response mutant that bears an allele of the ACTIN2 gene and shows altered actin configuration, PIN2 delocalization, and a broad array of phenotypes that recapitulate BR-treated plants. Moreover, we show that actin filament reconfiguration is sufficient to activate BR signaling, which leads to an enhanced auxin response. Our results demonstrate that the actin cytoskeleton functions as an integration node for the BR signaling pathway and auxin responsiveness.

A mutant of the Arabidopsis phosphate transporter PHT1;1 displays enhanced arsenic accumulation.

The exceptional toxicity of arsenate [As(V)] is derived from its close chemical similarity to phosphate (Pi), which allows the metalloid to be easily incorporated into plant cells through the high-affinity Pi transport system. In this study, we identified an As(V)-tolerant mutant of Arabidopsis thaliana named pht1;1-3, which harbors a semidominant allele coding for the high-affinity Pi transporter PHT1;1. pht1;1-3 displays a slow rate of As(V) uptake that ultimately enables the mutant to accumulate double the arsenic found in wild-type plants. Overexpression of the mutant protein in wild-type plants provokes phenotypic effects similar to pht1;1-3 with regard to As(V) uptake and accumulation. In addition, gene expression analysis of wild-type and mutant plants revealed that, in Arabidopsis, As(V) represses the activation of genes specifically involved in Pi uptake, while inducing others transcriptionally regulated by As(V), suggesting that converse signaling pathways are involved in plant responses to As(V) and low Pi availability. Furthermore, the repression effect of As(V) on Pi starvation responses may reflect a regulatory mechanism to protect plants from the extreme toxicity of arsenic.