Biology subjects

Morcillo, R.

Publications and source records attributed to Morcillo, R..

4 recordsLinked to original sources

bioRxiv2026

Acetic acid enhances tolerance to long-term water deficit in tomato by partially buffering transcriptomic and proteomic reprogramming independently of canonical jasmonate signalling

Acetic acid (AA), a volatile compound present in diverse microbial-derived biostimulants, enhances drought tolerance in plants. In Arabidopsis, soil-applied AA action has been linked to histone H4 acetylation and activation of jasmonate (JA) signalling. However, the mechanisms underlying AA action in crops of agronomic interest remain poorly understood. Here, we used an integrative approach to evaluate the effects of soil-applied AA on fruit yield, physiological performance, and leaf transcriptomic and proteomic profiles of tomato plants grown under optimal and suboptimal irrigation conditions (OIC and SOIC, respectively). While AA had little effect under OIC, it significantly enhanced fruit yield and photosynthesis under SOIC. Long-term water deficit triggered extensive transcriptomic and proteomic reprogramming, particularly affecting photosynthesis, RNA processing, protein biosynthesis-, modification- and homeostasis-related processes. Under SOIC, AA induced marked molecular changes that were not consistent with activation of canonical JA signaling pathways. Notably, only [~] 10% of the drought- or AA-responsive proteins were associated with corresponding transcript changes, highlighting a predominant role of regulatory layers beyond the transcriptional control to both long-term water deficit- and AA-induced protein remodeling. Strikingly, AA attenuated 47% and 35% of the transcriptomic and proteomic alterations induced by long-term water deficit, respectively. In addition, AA altered the abundance of numerous proteins that do not respond to drought, particularly ribosomal proteins and proteins involved in RNA processing. Collectively, our findings indicate that AA enhances tolerance to prolonged water deficit in tomato through mechanisms largely independent of canonical JA signaling and involving extensive downstream regulatory processes that partially mitigate stress-induced molecular reprogramming.

Plant Biology↗

bioRxiv2020

The Arabidopsis E3 ubiquitin ligase PUB4 regulates BIK1 homeostasis and is targeted by a bacterial type-III effector

Plant immunity is tightly controlled by a complex and dynamic regulatory network, which ensures optimal activation upon detection of potential pathogens. Accordingly, each component of this network is a potential target for manipulation by pathogens. Here, we report that RipAC, a type III-secreted effector from the bacterial pathogen Ralstonia solanacearum, targets the plant E3 ubiquitin ligase PUB4 to inhibit pattern-triggered immunity (PTI). PUB4 plays a positive role in PTI by regulating the homeostasis of the central immune kinase BIK1. Before PAMP perception, PUB4 promotes the degradation of non-activated BIK1, while, after PAMP perception, PUB4 contributes to the accumulation of activated BIK1. RipAC leads to BIK1 degradation, which correlates with its PTI-inhibitory activity. RipAC causes a reduction in pathogen-associated molecular pattern (PAMP)-induced PUB4 accumulation and phosphorylation. Our results shed light on the role played by PUB4 in immune regulation, and illustrate an indirect targeting of the immune signalling hub BIK1 by a bacterial effector.

plant biology↗

bioRxiv2019

Tomato root transformation followed by inoculation with Ralstonia solanacearum for straightforward genetic analysis of bacterial wilt disease

Ralstonia solanacearum is a devastating soil borne vascular pathogen that is able to infect a large range of plant species, causing an important threat to agriculture. However, the Ralstonia model is considerably under-explored in comparison to other models involving bacterial plant pathogens, such as Pseudomonas syringae in Arabidopsis. Research targeted to understanding the interaction between Ralstonia and crop plants is essential to develop sustainable solutions to fight against bacterial wilt disease, but is currently hindered by the lack of straightforward experimental assays to characterize the different components of the interaction in native host plants. In this scenario, we have developed an easy method to perform genetic analysis of Ralstonia infection of tomato, a natural host of Ralstonia. This method is based on Agrobacterium rhizogenes-mediated transformation of tomato roots, followed by Ralstonia soil-drenching inoculation of the resulting plants, containing transformed roots expressing the construct of interest. The versatility of the root transformation assay allows performing either gene overexpression or gene silencing mediated by RNAi. As a proof of concept, we used this method to show that RNAi-mediated silencing of SlCESA6 of tomato roots conferred resistance to Ralstonia. Here, we describe this method in detail, enabling genetic approaches to understand bacterial wilt disease in a relative short time and with small requirements of equipment and plant growth space.\n\nSUMMARYA versatile method for tomato root transformation followed by inoculation with Ralstonia solanacearum to perform straightforward genetic analysis for the study of bacterial wilt disease.

plant biology↗

bioRxiv2019

A bacterial effector protein prevents MAPK-mediated phosphorylation of SGT1 to suppress plant immunity

Nucleotide-binding domain and leucine-rich repeat-containing (NLR) proteins function as sensors that perceive pathogen molecules and activate immunity. In plants, the accumulation and activation of NLRs is regulated by SUPPRESSOR OF G2 ALLELE OF skp1 (SGT1). In this work, we found that an effector protein named RipAC, secreted by the plant pathogen Ralstonia solanacearum, associates with SGT1 to suppress NLR-mediated SGT1-dependent immune responses, including those triggered by another R. solanacearum effector, RipE1. RipAC does not affect the accumulation of SGT1 or NLRs, or their interaction. However, RipAC inhibits the interaction between SGT1 and MAP kinases, and the phosphorylation of a MAPK target motif in the C-terminal domain of SGT1. Such phosphorylation is enhanced upon activation of immune signaling, leads to the release of the interaction between SGT1 and NLRs, and contributes to the activation of NLR-mediated responses. Additionally, SGT1 phosphorylation contributes to resistance against R. solanacearum, and this is particularly evident in the absence of RipAC. Our results shed light onto the mechanism of activation of NLR-mediated immunity, and suggest a positive feedback loop between MAPK activation and SGT1-dependent NLR activation.

plant biology↗