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Summary   Xanthomonas campestris  pv.  campestris  ( Xcc ), the causal agent of black rot in crucifers, produces a membrane‐bound yellow pigment called xanthomonadin to protect against photobiological and peroxidative damage, and uses a quorum‐sensing mechanism mediated by the diffusible signal factor (DSF) family signals to regulate virulence factors production. The  Xcc  gene XCC4003, annotated as  Xcc fabG3 , is located in the  pig  cluster, which may be responsible for xanthomonadin synthesis. We report that  fabG3  expression restored the growth of the  Escherichia coli fabG  temperature‐sensitive mutant CL104 under non‐permissive conditions.  In vitro  assays demonstrated that FabG3 catalyses the reduction of 3‐oxoacyl‐acyl carrier protein (ACP) intermediates in fatty acid synthetic reactions, although FabG3 had a lower activity than FabG1. Moreover, the  fabG3  deletion did not affect growth or fatty acid composition. These results indicate that  Xcc fabG3  encodes a 3‐oxoacyl‐ACP reductase, but is not essential for growth or fatty acid synthesis. However, the  Xcc fabG3  knock‐out mutant abolished xanthomonadin production, which could be only restored by wild‐type  fabG3 , but not by other 3‐oxoacyl‐ACP reductase‐encoding genes, indicating that  Xcc  FabG3 is specifically involved in xanthomonadin biosynthesis. Additionally, our study also shows that the  Xcc fabG3 ‐disrupted mutant affects  Xcc  virulence in host plants.

A novel 3‐oxoacyl‐ACP reductase (FabG3) is involved in the xanthomonadin biosynthesis of Xanthomonas campestris pv. campestris