Ralf Müller-Xing

Autophagy restricts intracellular bacteria through xenophagy, yet many bacterial pathogens remodel this pathway to avoid degradation or support intracellular persistence. This review compares bacterial modulation of autophagy in mammalian cells and invertebrate vectors, with focusing on initiation, cargo recognition, autophagosome maturation, and autophagosome-lysosome fusion. In mammals, direct effector-host interactions have been defined for several pathogens. Legionella pneumophila RavZ effector removes lipidated ATG8/LC3 from autophagosome membranes. Salmonella typhimurium effectors interfere with AMPK-mTOR signaling, ATG16L1 recruitment, and Rab1A/TRAPPIII-dependent initiation. Shigella flexneri and Listeria monocytogenes mask bacterial surfaces to limit autophagic recognition. Mycobacterium tuberculosis, Anaplasma phagocytophilum, Staphylococcus aureus, and Coxiella burnetii exploit autophagy-related compartments while restricting degradative maturation. In invertebrate systems, especially psyllid vectors of Candidatus Liberibacter asiaticus and Candidatus Liberibacter solanacearum, current evidence indicates pathogen-associated changes in ATG gene expression, endoplasmic reticulum-associated vacuole formation, calcium and ROS signaling, lysosomal activity, and vitellogenin-linked regulation. However, these mechanisms are supported mainly by transcriptomic, microscopy-based, pharmacological, and protein-interaction evidence, and direct effector-mediated control of psyllid autophagy remains insufficiently demonstrated. We propose that bacterial control of autophagy follows conserved logic across host systems. This logic includes suppression of xenophagic recognition, remodeling of autophagosome biogenesis, and uncoupling of autophagosome formation from lysosomal dagradation. Defining which mechanisms are directly effector-driven and which are host-response signatures will be essential for translating autophagy biology into antimicrobial, vector-control, and plant disease-management strategies.

Autophagy is an evolutionarily conserved intracellular degradation pathway that has emerged as an important regulator of plant immunity and a recurrent target of pathogen virulence strategies. In this review, we examine how Candidatus Liberibacter (CL) species and their hosts provide a useful informative system for understanding convergent pathogen manipulation of the ATG6-ATG8 autophagic hub in agricultural and model plants. We synthesize recent evidence showing that CL-effectors reprogram autophagy through mechanistically distinct but functionally convergent strategies, including interference with ATG6- and ATG8-associated processes and exploitation of host metabolic regulators linked to autophagic flux. By comparing these mechanisms with autophagy targeting strategies reported for other plant-associated pathogens, we highlight recurring vulnerability nodes within the host autophagic machinery and suggest that these nodes may represent promising targets for future resistance engineering. We further discuss how structure guided molecular design and programmable genome editing could, over time, inform the development of more precise and durable approaches to crop protection.

Biological systems such as gene regulatory networks (GRNs) acquire robustness by feedback and feed-forward loops. Although many adaptations and robustness of biological systems seem to be implemented through feedback loops, feed-forward loops were demonstrated computationally and in synthetic biology applications to be as effective as feedback loops.

Plants have the capacity to form adventitious roots (ARs) from detached aerial organs, a process known as de novo root regeneration (DNRR). In Arabidopsis, wounding signals rapidly induce in leaf explants the expression of genes encoding enzymes of auxin biosynthesis, resulting in elevated auxin levels and facilitating AR formation. Here, we report that DEVELOPMENT-RELATED POLYCOMB TARGET IN THE APEX 4 (DPA4/NGAL3), a well-known regulator in seed size and leaf margin development, and a repressor of CUP-SHAPED COTYLEDON 2 (CUC2), inhibits AR formation in detached leaves. Leaf explants of dpa4-2 and cuc2-1D mutants displayed both elevated CUC2 mRNA levels and increased rooting rates. We observed reduced expression of ULTRAPETALA1 (ULT1), a negative regulator of DNRR, while the auxin biosynthesis genes ASA1, YUC4, and YUC9 were upregulated in both mutants. Through pharmacological inhibition of YUCCA-mediated auxin biogenesis, we obtained evidence that the enhanced AR formation in both mutants is at least partially a result of increased auxin production. Genetic analysis of dpa4-2 cuc2-1D double mutants indicates that similar mechanisms promote DNRR in both mutants. In summary, our study suggests that DPA4 suppresses AR formation likely by repression of CUC2 and activation of ULT1, which, in turn, suppresses endogenous auxin biogenesis and DNRR.

Plants have the capacity to form adventitious roots (ARs) from detached aerial organs, a process known as de novo root regeneration (DNRR). In Arabidopsis, wounding sig-nal rapidly induces in leaf explants the expression of genes encoding enzymes of auxin biosynthesis resulting in elevated auxin levels and facilitated AR formation. Here, we report that DEVELOPMENT-RELATED POLYCOMB TARGET IN THE APEX 4 (DPA4/NGAL3), a well-known regulator in seed size and leaf margin development, and repressor of CUP-SHAPED COTYLEDON 2 (CUC2), inhibits AR formation in de-tached leaves. Leaf explants of dpa4-2 and cuc2-1D mutants displayed both elevated CUC2 mRNA levels and increased rooting rates. We observed reduced expression of ULTRAPETALA1 (ULT1), a negative regulator of DNRR, while the auxin biosynthesis genes ASA1, YUC4, and YUC9 were upregulated in both mutants. Through pharmaco-logical inhibition of YUCCA-mediated auxin biogenesis, we obtained evidence that the enhanced AR formation in both mutants is at least partially a result of increased auxin production. Genetic analysis of dpa4-2 cuc2-1D double mutants indicates that similar mechanisms promotes DNRR in both mutants. In summary, our study suggests that DPA4 suppresses AR formation likely by repression of CUC2 and activation of ULT1, which, in turn, suppresses endogenous auxin biogenesis and DNRR.

Adventitious root (AR) formation in plants originates from non-root organs such as leaves and hypocotyls. Auxin signaling is essential for AR formation, but the roles of other phytohormones are less clear. In Arabidopsis, at least two distinct mechanisms can produce ARs, either from hypocotyls as part of the general root architecture or from wounded organs during de novo root regeneration (DNRR). In previous reports, gibberellin acid (GA) appeared to play reverse roles in both types of ARs, since GA treatment blocks etiolation-induced AR formation from hypocotyls, whereas GA synthesis and signaling mutants apparently displayed reduced DNRR from detached leaves. In order to clarify this contradiction, we employed the GA biosynthesis inhibitor paclobutrazol (PBZ) and found that PBZ had positive effects on both types of AR formation in Arabidopsis. Consistently, GA treatment had negative effects on both AR formation mechanisms, while loss of GA synthesis and signaling promoted DNRR under our conditions. Our results show that PBZ treatment can rescue declined AR formation in difficult-to-root leaf explants such as erecta receptor mutants. Furthermore, transcriptional profiling revealed that PBZ treatment altered GA, brassinosteroids, and auxin responses, which included the up-regulation of LBD16 that is well known for its pivotal role in AR initiation.

Adventitious root (AR) formation in plants origins from non-root organs such as leaves and hy-pocotyls. Auxin signaling is essential for AR formation, but the role of other phytohormones is less clear. In Arabidopsis, at least two distinct mechanisms can produce ARs either from hypocotyls as part of the general root architecture, or from wounded organs during de novo root regeneration (DNRR). In previous reports, gibberellin acid (GA) seems to play reverse roles in both types of AR formation, since GA treatment blocks AR formation from hypocotyls, whereas depletion of GA signaling results in reduced DNRR from detached leaves. Here, we report the positive effects of GA biosynthesis inhibitor paclobutrazol (PBZ/PAC) treatment on both types of AR formation in Arabidopsis. Consistently, loss of GA synthesis and signaling promoted DNRR in our conditions. Furthermore, PBZ treatment can rescue declined AR formation from leaf explants in erecta recep-tor mutants. Transcriptional profiling revealed that PBZ treatment altered GA, brassinosteroids and auxin responses, which included up-regulation of LBD16 that plays a pivotal role in AR initi-ation. This study reveals that depletion of GA biosynthesis promotes DNRR in Arabidopsis, and thus will contribute to further clarification of the role of GA during AR formation in plants.