**3. Defense Responses of GLS to Bacterial Diseases**

The bacteria that infect cruciferous plants are all rod-shaped bacteria, which can invade the host through stomata, hydathodes, and wounds, and then be retransmitted by running water, rain, insects, etc. Bacterial diseases in cruciferous have widespread occurrence, are highly destructive, and are challenging to control. Meanwhile, because the pathogens are different from the fungal diseases, the corresponding disease resistance mechanism of host and the GLS involved in resistance may be different. Several studies have demonstrated that GLS are involved in plant defense against a variety of bacterial diseases. Similar to the case in fungal disease infection, infection by *Burkholderia cepacia*, *Pseudomonas syringae*, and *Xanthomonas campestris* pv. *campestris* (*Xcc*) led to the upregulation of the GLS biosynthesis [99]. In addition, the introduction of CYP79 influenced *Arabidopsis* disease resistance by increasing the GLS synthesis, and overexpressing the CYP79D2 from cassava increased the accumulation of the aliphatic isopropyl and methylpropyl GLS, which also enhanced resistance against the soft-rot pathogen, *Erwinia carotovora*; however, overexpressing the sorghum CYP79A1 or CYP79A2 increased the accumulation of p-hydroxybenzyl and benzyl GLS, respectively [100].

Mishina et al. (2007) observed that the knockout of PAL1 increased leaf survival after *P. syringae* infection in an analysis conducted on *Arabidopsis* mutants and wild type plants, while Truman et al. (2007) and Aires et al. (2011) observed that indole GLS biosynthesis decreased after *P. syringae* infection [101–103]. Following the transcriptional and metabolic profiling of *A. thaliana* mutants, Clay et al. (2009) reported that the PEN2 and PEN3 genes are necessary for resistance to PtoDC3000 pathogens [104]. Furthermore, Geng et al. (2012) demonstrated that coronatine, a toxin produced by *P. syringae*, suppresses the salicylic acid (SA)-independent pathway, facilitating callose deposition by reducing the accumulation of an indole GLS upstream of the PEN2 myrosinase activity [105]. In addition, a positive correlation has been reported between total GLS content and *Xcc* disease severity, and *Xcc* infection enhanced GLS biosynthesis during the early infection period [106,107]. *Pectobacterium carotovorum* ssp. *carotovorum* infection in *B. rapa* can trigger the upregulation of the JA and ethylene (ET) biosynthesis genes in sr gene mutants and increase resistance capacity via GLS accumulation [108].
