BEGIN:VCALENDAR
VERSION:2.0
PRODID:-//ZContent.net//ZapCalLib 1.0//EN
CALSCALE:GREGORIAN
METHOD:PUBLISH
BEGIN:VEVENT
SUMMARY:HopBA1: A Bacterial Protein Acting at the Intersection of Plant Def
 ense and Development
LOCATION:Biology 133
TZID:America/Denver
DTSTART:20240408T090000
UID:2026-05-11-20-25-52@natsci.colostate.edu
DTSTAMP:20260511T202552
Description:Plant pathogens represent a major threat to food security as th
 ey dramatically reduce crop yield\, impact the expression of desirable tra
 its\, and reduce post-harvest longevity. Plant pathogens like Pseudomonas 
 syringae pv. tomato DC3000 (Pst) utilize a type III secretion system to de
 liver virulence proteins (effectors) into the cytoplasm of infected hosts 
 to suppress host immunity. In response\, plants have evolved intracellular
  immune receptors to perceive immunosuppression. Thus\, a given pathogen e
 ffector can both suppress and activate immunity depending on the host geno
 me.\n\nThe present work reveals an uncharacterized role for Pst as an aggr
 essive vascular pathogen\, causing systemic infection in the model plant N
 icotiana benthamiana (Nb). Further\, it establishes that the bacterial eff
 ector HopBA1 inhibits movement into the vascular system\, despite apparent
  virulence within the primary infection of leaves. Simultaneously\, HopBA1
  was found to rapidly induce vertical bending (hyponasty) in petioles of i
 nfiltrated leaves\, a novel phenotype for a bacterial effector. LC-MS/MS a
 nd RNA-Seq revealed phytohormone alteration (most significantly\, a reduct
 ion in auxin and Jasmonic acid-related metabolites) and transcriptional re
 programming of developmental and defense genes not associated with Pst alo
 ne. Since Pst + HopBA1 resulted in vascular-specific bacterial growth rest
 riction\, a suite of Nb immune receptor mutants were screened for loss of 
 HopBA1-induced hyponasty. Interestingly\, bacterial growth was restored to
  Pst + empty vector levels in Nb eds1-/- (Enhanced Disease Resistance1) pl
 ants\, which still undergo HopBA1-induced hyponasty. Together\, these resu
 lts imply a form of vascular-specific effector-triggered immunity (ETI) an
 d suggest that hyponasty is due to HopBA1’s biochemical activity\, rathe
 r than host recognition. Thus\, HopBA1 delivery by the model pathogen Pst 
 becomes an important tool to dissect a poorly understood area of disease r
 esistance\, specifically the genetic and molecular basis of vascular ETI. 
 9:00 am
END:VEVENT
END:VCALENDAR