Environmental cues profoundly modulate cell proliferation and cell elongation to inform and direct plant growth and development. External phosphate (Pi) limitation inhibits primary root growth in many plant species. However, the underlying Pi sensory mechanisms are unknown. Here we genetically uncouple two Pi sensing pathways in the root apex of Arabidopsis thaliana. First, the rapid inhibition of cell elongation in the transition zone is controlled by transcription factor STOP1, by its direct target, ALMT1, encoding a malate channel, and by ferroxidase LPR1, which together mediate Fe and peroxidase-dependent cell wall stiffening. Second, during the subsequent slow inhibition of cell proliferation in the apical meristem, which is mediated by LPR1-dependent, but largely STOP1–ALMT1-independent, Fe and callose accumulate in the stem cell niche, leading to meristem reduction. Our work uncovers STOP1 and ALMT1 as a signalling pathway of low Pi availability and exuded malate as an unexpected apoplastic inhibitor of root cell wall expansion.

Lacking an adaptive immune system, plants rely on innate immunity comprising two main layers: PAMP-triggered immunity (PTI) and effector-triggered immunity (ETI), both utilizing Ca²⁺ influx and reactive oxygen species (ROS) for signaling. PTI, mediated by pattern-recognition receptors (PRRs), responds to conserved pathogen- or damage-associated molecular patterns. Some pathogens evade PTI using effectors, triggering plants to activate ETI. At the heart of ETI are nucleotide-binding leucine-rich repeat receptors (NLRs), which detect specific pathogen effectors and initiate a robust immune response. NLRs, equipped with a nucleotide-binding domain and leucine-rich repeats, drive a potent immune reaction starting with pronounced, prolonged cytosolic Ca²⁺ influx, followed by increased ROS levels. This sequence of events triggers the hypersensitive response-a localized cell death designed to limit pathogen spread. This intricate use of Ca²⁺ and ROS highlights the crucial role of NLRs in supplementing the absence of an adaptive immune system in plant innate immunity.

Summary: To cause disease in lettuce, the biotrophic oomycete Bremia lactucae secretes potential RxLR effector proteins. Here we report the discovery of an effector‐target hub consisting of four B. lactucae effectors and one lettuce protein target by a yeast‐two‐hybrid (Y2H) screening. Interaction of the lettuce tail‐anchored NAC transcription factor, LsNAC069, with B. lactucae effectors does not require the N‐terminal NAC domain but depends on the C‐terminal region including the transmembrane domain. Furthermore, in Y2H experiments, B. lactucae effectors interact with Arabidopsis and potato tail‐anchored NACs, suggesting that they are conserved effector targets. Transient expression of RxLR effector proteins BLR05 and BLR09 and their target LsNAC069 in planta revealed a predominant localization to the endoplasmic reticulum. Phytophthora capsici culture filtrate and polyethylene glycol treatment induced relocalization to the nucleus of a stabilized LsNAC069 protein, lacking the NAC‐domain (LsNAC069^ΔNAC). Relocalization was significantly reduced in the presence of the Ser/Cys‐protease inhibitor TPCK indicating proteolytic cleavage of LsNAC069 allows for relocalization. Co‐expression of effectors with LsNAC069^ΔNAC reduced its nuclear accumulation. Surprisingly, LsNAC069 silenced lettuce lines had decreased LsNAC069 transcript levels but did not show significantly altered susceptibility to B. lactucae. In contrast, LsNAC069 silencing increased resistance to Pseudomonas cichorii bacteria and reduced wilting effects under moderate drought stress, indicating a broad role of LsNAC069 in abiotic and biotic stress responses.

Summary: Pathogens use effectors to suppress host defence mechanisms, promote the derivation of nutrients, and facilitate infection within the host plant. Much is now known about effectors that target biotic pathways, particularly those that interfere with plant innate immunity. By contrast, an understanding of how effectors manipulate nonimmunity pathways is only beginning to emerge. Here, we focus on exciting new insights into effectors that target abiotic stress adaptation pathways, tampering with key functions within the plant to promote colonization. We critically assess the role of various signalling agents in linking different pathways upon perturbation by pathogen effectors. Additionally, this review provides a summary of currently known bacterial, fungal, and oomycete pathogen effectors that induce biotic and abiotic stress responses in the plant, as a first step towards establishing a comprehensive picture for linking effector targets to pathogenic lifestyles.