The search for environmentally friendly solutions to effectively control crop pests while safeguarding human health has become a global priority. One promising strategy is to enhance plant defenses by pre-inducing their innate immune system. In this study, we developed rhamnolipid (RL)-stabilized nanoemulsions (NEs) encapsulating essential oils (EOs) as potential biopesticides and biostimulants for agroindustrial applications. These NEs were designed to improve the solubility and stability of EOs while effectively combining their insecticidal and/or repellent activities with the bioactive properties of RLs. In this regard, our interdisciplinary approach involved formulating and characterizing these NEs and evaluating their stability and wettability on plant leaf surfaces. We further evaluated their effects on bacterial growth in vitro and in the model plant Arabidopsis thaliana, along with their impact on beneficial soil microorganisms. We analyzed their ability to stimulate the plant’s immune system and their impact on the viability and reproduction of the aphid Myzus persicae. Additionally, we explored whether RLs stimulate plant defenses through alterations in the leaf cuticle. Our findings demonstrate that RL-stabilized EO-NEs are effective bioprotectants and biostimulants in the model plant, offering a sustainable alternative that could reduce reliance on chemical pesticides in agriculture.

StarD7 belongs to START protein family involved in lipid traffic, metabolism, and signaling events. Its precursor, StarD7.I which is important for mitochondrial homeostasis, is processed to the StarD7.II isoform that lacks the mitochondrial targeting sequence and is mainly released to the cytosol. StarD7 knockdown interferes with cell migration by an unknown mechanism. Here, we demonstrate that StarD7 silencing decreased connexin 43 (Cx43), integrin β1, and p-ERK1/2 expression in the non-tumoral migratory HTR-8/SVneo cells. StarD7-deficient cells exhibited Golgi disruption and reduced competence to reorient the microtubule-organizing center. The migratory capacity of StarD7-silenced cells was reestablished when Cx43 level was resettled, while p-ERK1/2 expression remained low. Importantly, ectopic expression of the StarD7.II isoform not only restored cell migration but also ERK1/2, Cx43, and integrin β1 expression. Thus, StarD7 is implicated in cell migration through an ERK1/2/Cx43 dependent mechanism but independent of the StarD7.I function in the mitochondria.

Filamentous pathogens, such as oomycetes, employ multiple strategies to suppress plant immunity, one of which involves manipulating phytohormone signaling pathways. The effector HaRxL106 from Hyaloperonospora arabidopsidis (Hpa), known to induce shade avoidance syndrome (SAS)-like growth, has previously been shown to interact with brassinosteroid signaling components. Here, we investigate the role of HaRxL106 in altering auxin signaling, revealing that HaRxL106 targets the AUX/IAA protein IAA11, a key negative regulator of auxin responses. Our data suggest that HaRxL106 impedes the repressive function of IAA11, enhancing auxin signaling and promoting SAS, which concurrently suppresses plant immune responses. These findings provide insights into how pathogen effectors manipulate plant growth and immunity to facilitate infection.

Hyaloperonospora arabidopsidis (Hpa) is an oomycete pathogen that causes downy mildew disease on Arabidopsis. This obligate biotroph manipulates the homeostasis of its host plant by secreting numerous effector proteins, among which are the RxLR-effectors. Identifying the host targets of effectors and understanding how their manipulation facilitates colonization of plants is key to improve plant resistance to pathogens. Here we characterize the interaction between the RxLR effector HaRxL106 and BIM1, an Arabidopsis transcription factor (TF) involved in Brassinosteroid (BR) signaling. We report that HaRxL106 interacts with BIM1 in vitro and in planta. BIM1 is required by the effector to increase the host plant susceptibility to (hemi)biotrophic pathogens, and thus can be regarded as a susceptibility factor. Mechanistically, HaRxL106 requires BIM1 to induce the transcriptional activation of BR-responsive genes and cause alterations in plant growth patterns that phenocopy the shade avoidance syndrome. Our results support previous observations of antagonistic interactions between activation of BR signaling and suppression of plant immune responses and reveal that BIM1, a new player in this crosstalk, is manipulated by the pathogenic effector HaRxL106. SIGNIFICANCE STATEMENT Our study reveals that the Arabidopsis transcription factor BIM1 plays a key role as a susceptibility factor that is manipulated by the oomycete effector HaRxL106 to induce the Brassinosteroid (BR) signaling pathway and suppress plant immunity. HaRxL106 induces BIM1-dependent expression of BR-responsive genes which affects normal plant growth generating a shade avoidance-like syndrome that impacts negatively on plant defenses against bacterial and oomycete pathogens.

Filamentous pathogens, such as oomycetes, employ multiple strategies to suppress plant immunity, including manipulation of phytohormone signalling pathways. The effector HaRxL106 from the oomycete Hyaloperonospora arabidopsidis (Hpa), whose expression in planta induces shade avoidance syndrome (SAS)-like growth, has previously been shown to interact with BIM1, a transcription factor involved in brassinosteroid signalling. Here, we present evidence that HaRxL106 interacts with another key host target, the AUX/IAA protein IAA11, a negative regulator of auxin responses. Our data suggest that HaRxL106 may impede the repressive function of IAA11, affecting auxin signalling, which in coordination with an enhanced brassinosteroid output suppresses plant immune responses. These findings provide insights into how pathogen effectors manipulate plant growth and immunity to facilitate infection.