Skip to main content
ISMPMI Congress 2025 Main banner
Icon Legend
This session is not in your schedule.
This session is in your schedule. Click again to remove it.

Concurrent Session

Session: Concurrent Session: Effector Interference Mechanisms

Effector crosstalk in Xanthomonas citri: host ripening pathway links type III and type II effector virulence functions

Tuesday, July 15, 2025
11:50 - 12:10  
Location: Room M+N

Virulence of the citrus canker pathogen Xanthomonas citri ssp. citri (Xcc) depends on the type III effector (T3E) PthA4, which activates the host transcription factor CsLOB1. To understand how CsLOB1 promotes bacterial growth, we combined RNA-seq and ChIP-seq and identified ~100 direct CsLOB1 target genes, many encoding plant cell wall-degrading enzymes (CWDEs). We defined and validated a conserved CsLOB1-binding motif, also recognized by its tomato ortholog SlLOB1. Since SlLOB1 is active during fruit ripening, we examined CsLOB1 and found it similarly expressed in citrus fruit. This parallel suggests CsLOB1, like SlLOB1, regulates a ripening-associated regulon. We propose that PthA4 hijacks this program in leaves to activate CWDEs and release wall sugars for pathogen use. RNA-seq of in planta-grown wild-type Xcc and a PthA4-deficient mutant revealed that PthA4 also activates a xylan-specific carbohydrate utilization (CUT) system in Xcc. This includes a xylanase secreted via the type II secretion system (T2SS), likely acting with host CWDEs to degrade xylan, a major hemicellulose component. Thus, by reprogramming the host, PthA4 indirectly promotes T2 effector function. This finding contrasts with the prevailing model where T3Es suppress immune responses triggered by T2Es. Instead, we uncover a cooperative mechanism in which a T3E enables T2E deployment by shaping a permissive metabolic niche, revealing an unexpected layer of effector synergy in bacterial virulence.