Unveiling the Nature of Survival: A New Trade-Off Between Plant Reproduction and Defence

Abstract

Plants participate in a broad range of mutualistic and antagonistic interactions with species that have important ecological and evolutionary impacts (Rodelius and Iler 2025). In nature, microorganisms are considered the primary invaders, dominating host-pathogen interactions and leading to disease occurrence (Escalante et al. 2024). Interestingly, plants maintain a delicate balance between growth and immunity by activating their defence systems in response to stress factors, including microorganisms and environmental pressures (Meijer et al. 2024). For example, plants experience a trade-off between reproduction and survival under environmental stress, especially during ovule initiation (James and Geber 2025; Yang et al. 2025). As the core structure for the reproduction of seed plants and the maintenance of ecosystems, this step determines the maximum number of seeds in one fruit and has a great impact on total seed yield (Rudall 2021).

Pathogen infection is primarily recognised for its pathological effects on host plants, but the potential impacts of non-adapted pathogens on nonhost plants have rarely been explored. Yang et al. (2025) raised an important scientific question: how do non-adapted bacteria influence the reproductive development of nonhost plants? This study revealed that PXO99A infection in the nonhost plant Arabidopsis suppressed ovule development and reduced seed numbers, without causing visible pathological symptoms. Yang et al. (2025) introduced the direct effects of bacterial effector proteins on plant reproductive organs, bridging a critical gap in knowledge of plant reproductive development and plant pathology. This study provides a new perspective on the trade-off between plant growth and development, and environmental adaptation. It not only enhances our understanding of the interactions between non-adapted pathogens and nonhost plants, but also reveals the trade-off mechanisms between reproduction and defence in plants under environmental stress.

Yang et al. (2025) found that infection of Arabidopsis flowers by Xanthomonas oryzae pv. oryzae PXO99A did not cause obvious disease symptoms, but was able to suppress ovule initiation and result in a reduction in seed number. Analysis of the secretion system of strain PXO99A revealed that the effector TleB in the type VI secretion system directly inhibits ovule initiation in Arabidopsis, which is a major discovery in the understanding of bacterial-plant interactions. PUB14, an E3 ubiquitin ligase, was identified, which binds and polyubiquitinates TleB and promotes its degradation via the 26S proteasome, thereby reducing plant damage from TleB invasion. Meanwhile, the authors found that the BZR1 protein and its family of downstream genes were significantly altered after PXO99A treatment and suggested that PXO99A reduces the stability of BZR1 protein in the ovule, with TleB playing a key role in this process. To explore the relationship between TleB, PUB14, and BZR1, the authors hypothesised that a functional link exists between the three. Bimolecular fluorescence complementation (BiFC) and co-immunoprecipitation (co-IP) assays revealed that PUB14 and BZR1 interact during ovule initiation.

To validate the function of PUB14, Yang et al. (2025) also constructed a PUB14 CRISPR line and an overexpression line, UBQ10:PUB14-mCherry. The results showed that the number of seeds and ovules in the plants increased significantly with increasing PUB14 expression, and the BZR1 protein level, as well as the expression of genes related to ovule initiation, also increased. Therefore, PUB14 promotes ovule initiation by stabilising the positive regulator BZR1.

Although PUB14 stabilises BZR1 and enhances ovule initiation, PUB14 induction in response to TleB does not promote or may even inhibit ovule initiation. Therefore, TleB may disrupt the interaction between PUB14 and BZR1 by competitively binding to PUB14, thereby inhibiting ovule initiation (Figure 1). A very important contribution of the article by Yang et al. (2025) was to provide evidence that PUB14 interacts with and stabilises BZR1 to promote ovule initiation in the absence of bacterial infection. When non-pathogenic bacteria infect plants, TleB competitively inhibits this interaction between PUB14 and BZR1, and the released and newly generated PUB14 binds to and degrades the TleB effector; meanwhile, when PUB14 does not bind to BZR1, the level of BZR1 protein decreases, which leads to a reduction in the number of ovules.

Previous research has primarily focused on how pathogens infect plants to understand their effects on plant growth and development (Lo Presti et al. 2015). For example, the bacterial wilt disease is caused by the plant pathogen Ralstonia (Meline et al. 2023). Phytophthora infestans is an oomycete plant pathogen responsible for the potato famine (Sabbadin et al. 2021). For non-pathogens, such as arbuscular mycorrhizal fungi (AMF), previous studies have shown that AMF infect nonhost plants, rob nutrients, inhibit the growth and development of nonhost plants, and form a symbiotic relationship with host plants (Wang et al. 2023). However, the interactions between bacteria and nonhost plants remain unexplored. Yang et al. (2025) proposed that the suppression of ovule development in plants during bacterial infection may be a “survival mode”, in which resources are stored by reducing reproductive investment, thereby enhancing resistance. This model provides a new perspective on plant adapted strategies when facing adverse environments. Overall, this study provide a strong framework for understanding the trade-offs between plant growth, development, and environmental adaptation under environmental stress, laying a solid foundation for future research on plant resistance improvement and ecological adaptability.

The authors declare no conflicts of interest.