Spatiotemporal reprogramming of auxin signaling and resistance outputs across model plants and solanaceae crops under Ralstonia solanacearum infection.

Bacterial wilt is a devastating vascular disease caused by the soil-borne bacterium Ralstonia solanacearum, which invades and blocks the xylem of susceptible plants, especially economically important solanaceous crops. In addition to classical plant defense hormones, recent research has focused on understanding the role of auxin as a key and continuous regulator of infection and development. Auxin connects changes during infection to root development and the progression of bacterial wilt disease. The auxin related shift in plant hormone patterns associated with root development has been observed in both infected and non-infected host plant species. This shift is accompanied by the upregulation of several auxin regulating transcriptional programs, the accumulation of indole-3-acetic acid, and the enhancement of auxin signaling in specific plant tissues. The auxin-associated reprogramming of roots infected with R. solanacearum is also linked to the reorganization of root developmental programs, including reduced primary root elongation, pronounced induction of root hair formation, and increased lateral root development at later stages of infection. Root hair formation in response to infection requires an intact and functional auxin signaling pathway. There is also support for a positive relationship between the level of auxin responsiveness and a plant's susceptibility to infection. Susceptible genotypes activate their auxin pathway more than resistant genotypes, while reducing the ability to transport or perceive auxin increases plant resistance and decreases the severity of key root-associated phenotypes during infections. At the molecular level, R. solanacearum is reported to influence the auxin homeostasis of the host plant indirectly through effectors, which induce changes in the plant immune response, alter metabolism and energy status, and modify the interactions within plant hormone pathways. These changes create conditions that facilitate the colonization and spread of R. solanacearum. Therefore, auxin is best understood as a dynamically regulated "balancer" that mediates the trade-off between plant growth and defense, integrating the plant developmental flexibility with immune response. Furthermore, leveraging these findings to develop precision resistance offers strategies for enhancing plant resistance. These include improving auxin modulation within the growth environment and employing spatiotemporal transcriptomics to identify spatially and temporally correlated losses of auxin sensitivity or transport in root zones susceptible to infection.