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With an increasing demand for renewable fuels, bioenergy crops are being developed with high sugar content and altered cell walls to improve processing efficiency. These traits may have unintended consequences for plant disease resistance. Xanthomonas vasicola pv. holcicola ( Xvh ), the causal agent of sorghum bacterial leaf streak, is a wide-spread bacterial pathogen. Here, we show that Xvh expresses several bacterial cell wall degrading enzymes (CWDEs) during sorghum infection, and these are required for full virulence. In tolerant sorghum, Xvh infection results in induction of a key enzyme in monolignol biosynthesis, Brown midrib 12 ( Bmr12 ), but this did not affect lignin content nor composition. Mutation of Bmr12 rendered the tolerant genotype susceptible. Bmr12 encodes caffeic acid O -methyltransferase (COMT), an enzyme that generates sinapaldehyde as its major product. Growth inhibition of Xvh in the presence of sinapaldehyde was observed in vitro. We conclude that mutations that alter the components of the sorghum cell wall can reduce sorghum resistance to Xvh and that Xvh CWDEs contribute to bacterial virulence. Given the enhanced bioprocessing characteristics of bmr12 sorghum, these results provide a cautionary tale for current and future efforts aimed at developing dedicated bioenergy crops.

The plant hormone indole-3-acetic acid (IAA), also known as auxin, plays important roles in plant growth and development, as well as in several plant-microbe interactions. IAA also acts as a microbial signal and in many bacteria regulates metabolism, stress responses, and virulence. In the bacterial plant pathogen Pseudomonas syringae pv. tomato strain DC3000 ( Pto DC3000), exposure to IAA results in large-scale transcriptional reprogramming, including the differential expression of several known virulence genes. However, how Pto DC3000 senses and responds to IAA and what aspects of its biology are regulated by IAA is not understood. To investigate the mechanisms involved in perceiving and responding to IAA, we carried out a genetic screen for mutants with altered responses to IAA. One group of mutants of particular interest carried disruptions in the aefR gene encoding a TetR family transcriptional regulator. Gene expression analysis confirmed that the aefR mutants have altered responses to IAA. Thus, AefR is the first demonstrated auxin response regulator in Pto DC3000. We also investigated several aspects of Pto DC3000 biology that are regulated by both AefR and IAA, including antibiotic resistance, motility, and virulence. The observation that the aefR mutant has altered virulence on Arabidopsis , suggests that the sector of the IAA response regulated by aefR is important during pathogenesis. Our findings also provide evidence that AefR plays a role in coordinating changes in gene expression during the transition from early to late stages of infection. [Formula: see text] Copyright © 2024 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license., Competing Interests: The author(s) declare no conflict of interest.

The plant hormone auxin governs many aspects of normal plant growth and development. Auxin also plays an important role in plant-microbe interactions, including interactions between plant hosts and pathogenic microorganisms that cause disease. It is now well established that indole-3-acetic acid (IAA), the most well-studied form of auxin, promotes disease in many plant-pathogen interactions. Recent studies have shown that IAA can act both as a plant hormone that modulates host signaling and physiology to increase host susceptibility and as a microbial signal that directly impacts the pathogen to promote virulence, but large gaps in our understanding remain. In this article, we review recent studies on the roles that auxin plays during plant-pathogen interactions and discuss the virulence mechanisms that many plant pathogens have evolved to manipulate host auxin signaling and promote pathogenesis., (Copyright © 2021 Cold Spring Harbor Laboratory Press; all rights reserved.)