Biology subjects

Cecchini, N. M.

Publications and source records attributed to Cecchini, N. M..

5 recordsLinked to original sources

bioRxiv2026

Alarmone ((p)ppGpp) signalling tunes Arabidopsis thaliana nuclear gene expression to shape the balance of plant immune outcomes

RSH enzymes (RelA/SpoT homologs) synthesize ppGpp (guanosine tetra-/pentaphosphate) in plastids, regulating organelle function. More importantly, whether ppGpp acts as a simple rheostat on immune output or determines which mode of defence a plant deploys remains poorly understood. Using Arabidopsis thaliana lines with high (RSH3OX) or null (rshq) ppGpp levels, we show that ppGpp controls nuclear-encoded defence genes in salicylic acid (SA) and jasmonic acid (JA) metabolism, including hormone-inactivating enzymes in RSH3OX and MeSA-to-SA conversion genes in rshq. Conversely, pathogen infection induces the ppGpp synthases RSH2 and RSH3, with induction preceding defence gene activation and requiring SA biosynthesis and a functional Type III secretion system. RSH3OX plants are hypersusceptible to Pseudomonas syringae pv. tomato DC3000, show impaired pattern-triggered immunity, and exhibit an accelerated decline in photosynthetic efficiency, while rshq plants show enhanced resistance to P. syringae but increased susceptibility to the necrotrophic fungus Botrytis cinerea. Using an inducible line to acutely elevate ppGpp, we confirm this susceptibility is directly caused by ppGpp levels, not a chronic developmental consequence of RSH3OX. Together, these results indicate that ppGpp governs the mode of immune execution rather than simply scaling its magnitude, acting as a chloroplast-based checkpoint linking organellar status to the nuclear defence transcriptome.

plant biology↗

bioRxiv2026

Selective autophagy promotes bacterial immunity under warming through NBR1-dependent regulation of ABI5

Elevated temperatures compromise plant immunity and increase susceptibility to bacterial pathogens through extensive reprogramming of hormone signaling pathways. Although autophagy contributes to both stress adaptation and pathogen defense, its role in hormone-dependent immune regulation under warm conditions remains unclear. Here, we investigated the contribution of NBR1 (NEIGHBOR OF BRCA1 GENE 1)-mediated selective autophagy to Arabidopsis immunity against Pseudomonas cannabina pv. alisalensis at elevated temperature. Bacterial infection under warming enhanced autophagic flux and promoted NBR1 turnover, indicating increased autophagic activity. Analysis of atg5 and nbr1 mutants, and NBR1-overexpressing lines, demonstrated that both core autophagy and NBR1-mediated selective autophagy contribute to bacterial immunity under warm conditions. Hormone and gene expression analyses indicated that NBR1 negatively regulates abscisic acid (ABA)-associated transcriptional responses during infection, while salicylic acid signaling was largely unaffected. Mechanistically, NBR1 physically associated with the ABA-responsive transcription factor ABI5 (ABA INSENSITIVE 5) and promoted its autophagy-dependent turnover in planta. ABI5 turnover was strongly reduced under warm conditions, leading to its accumulation in nbr1 and atg5 plants. Consistent with a functional role for ABI5 in this phenotype, genetic disruption of ABI5 largely reversed the increased susceptibility of nbr1 mutants at elevated temperature, whereas ABI5 overexpression increased susceptibility to bacterial infection. Together, our results identify NBR1-mediated selective autophagy as a regulatory mechanism that restrains ABA-associated susceptibility through the autophagy-dependent turnover of ABI5. These findings reveal a previously unrecognized connection between selective autophagy and ABA-dependent immune regulation and identify NBR1-mediated ABI5 turnover as a temperature-dependent mechanism that prevents stronger bacterial susceptibility under warm conditions.

plant biology↗

bioRxiv2025

Systemic resistance to pathogens in Arabidopsis requires HASTY-dependent miRNA cell-to-cell movement.

Plant defenses against pathogens are tightly regulated through complex gene expression control mechanisms. The precise activation and repression of defense-related genes are crucial to balancing the trade-off between growth and immunity. Micro RNAs (miRNAs) play a well-established role in the local regulation of plant-microbe interactions. While some miRNAs are also essential for systemic defense responses, their mechanisms of action, biogenesis, and long-distance mobility remain largely unexplored. Here, we show that HASTY (HST), a key factor in miRNA biogenesis and intercellular movement, is required for systemic defense activation. The impaired mobility of miRNAs in hst mutants correlates with a lack of systemic responses. In infected tissues, HST may enhance the co-transcriptional processing of specific pri-miRNAs, which promotes the cell-to-cell movement of their mature miRNAs and contributes to the activation of systemic defenses. Furthermore, two miRNAs that exhibit increased mobility during systemic defense induction are required for a proper systemic response. Interestingly, complementing hst mutants with a version of HST expressed exclusively in companion cells is sufficient to restore systemic defense induction, highlighting the role of miRNA cell-to-cell movement. These findings shed light on the role of HST in plant immunity, linking miRNA biogenesis and mobility to the fine-tuned regulation of systemic defenses.

molecular 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↗

bioRxiv2021

Friend or Foe: Hybrid proline-rich proteins determine how plants interact with and respond to beneficial and pathogenic microbes

Plant plastids generate signals, including some derived from lipids, that need to be mobilized to effect signaling. We used informatics to discover potential plastid membrane proteins involved in microbial responses. Among these are proteins co-regulated with the systemic immunity component AZI1, a hybrid proline-rich protein (HyPRP) and HyPRP superfamily members. HyPRPs have a transmembrane domain, a proline-rich region (PRR) and a lipid transfer protein domain. The precise subcellular location(s) and function(s) is unknown for most HyPRP family members. As predicted by informatics, a subset of HyPRPs have a pool of protein that targets plastid outer envelope membranes (OEMs) via a mechanism that requires the PRR. Additionally, two HyPRPs may be associated with thylakoid membranes. Most of the plastid and non-plastid localized family members also have pools that localize to endoplasmic reticulum, plasma membrane or plasmodesmata. HyPRPs with plastid pools regulate, positively or negatively, systemic immunity against the pathogen Pseudomonas syringae. HyPRPs also regulate the interaction with the plant growth promoting rhizobacteria Pseudomonas simiae WCS417 in the roots to influence colonization, root system architecture and/or biomass. Thus, HyPRPs have broad and distinct roles in immune, development and growth responses to microbes and reside at sites that may facilitate signal molecule transport.

plant biology↗