Flash – New biotechnological tools

Stomata are microscopic pores mainly located in leaf epidermis, allowing gas exchanges between plants and atmosphere. Stomatal initiation relies on the transcription factor SPEECHLESS which is mainly regulated by the MAP kinase cascade, in turn controlled by small signaling peptides, the Epidermal Patterning Factors (EPF and EPF-Like), namely EPF1, EPF2 and EPFL9. While EPF1 and EPF2 induce the inhibition of SPEECHLESS, their antagonist, EPFL9, stabilizes it, leading to stomatal formation. In grapevine, there are two paralogs for EPFL9, VviEPFL9-1 and VviEPFL9-2. Despite their structural similarity, it remains unclear whether they are differentially regulated and have distinct roles.

Climate change presents increasing challenges to viticulture, particularly with rising water stress contributing significantly to yield losses and damages. The identification of the MYB60 transcription factor, which regulates stomatal opening and closing in Arabidopsis thaliana and Vitis vinifera, offers potential solutions. Notably, knockout studies in Arabidopsis have shown reduced stomatal opening and increased drought tolerance in myb60 mutants. Additionally, the grapevine ortholog, VviMYB60, can restore the wild-type phenotype of Arabidopsis myb60 mutants. Further investigation of the Arabidopsis promoter region has revealed that mutations in DOF motifs lead to reduced expression of AtMYB60.

One of the main plant defence mechanisms is the Systemic Acquired Resistance (SAR) mediated by Salicylic Acid (SA). This is a heightened and broad-spectrum immune response initiated by the exposure to pathogens, inducing resistance not only in the infected site, but also throughout the entire plant. It was demonstrated that plant immune system can be regulated by two classes of SA receptors: NONEXPRESSOR OF PR GENES 1 (NPR1) and NPR1-LIKE PROTEIN 3 and 4 (NPR3/NPR4). While NPR1 is required for SA-induction followed by the expression of pathogenesis-related (PR) protein and resistance against pathogens, NPR3/NPR4 serve as transcriptional co-repressors of SA-responsive genes.