Open AccessPolar auxin transport is essential for gall formation by P antoea agglomerans on gypsophila
Author(s) -
Chalupowicz Laura,
Weinthal Dan,
Gaba Victor,
Sessa Guido,
Barash Isaac,
ManulisSasson Shulamit
Publication year - 2013
Publication title -
molecular plant pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.945
H-Index - 103
eISSN - 1364-3703
pISSN - 1464-6722
DOI - 10.1111/j.1364-3703.2012.00839.x
Subject(s) - auxin , biology , effector , gall , apical dominance , secretion , virulence , mutant , agrobacterium tumefaciens , microbiology and biotechnology , lanolin , botany , biochemistry , chemistry , gene , shoot , transgene , organic chemistry
Summary The virulence of the bacterium P antoea agglomerans pv. gypsophilae ( P ag ) on G ypsophila paniculata depends on a type III secretion system ( T3SS ) and its effectors. The hypothesis that plant‐derived indole‐3‐acetic acid ( IAA ) plays a major role in gall formation was examined by disrupting basipetal polar auxin transport with the specific inhibitors 2,3,5‐triiodobenzoic acid ( TIBA ) and N ‐1‐naphthylphthalamic acid ( NPA ). On inoculation with P ag , galls developed in gypsophila stems above but not below lanolin rings containing TIBA or NPA , whereas, in controls, galls developed above and below the rings. In contrast, TIBA and NPA could not inhibit tumour formation in tomato caused by A grobacterium tumefaciens . The colonization of gypsophila stems by P ag was reduced below, but not above, the lanolin– TIBA ring. Following P ag inoculation and TIBA treatment, the expression of hrp L (a T3SS regulator) and pag R (a quorum‐sensing transcriptional regulator) decreased four‐fold and that of pth G (a T3SS effector) two‐fold after 24 h. Expression of PIN2 (a putative auxin efflux carrier) increased 35‐fold, 24 h after P ag inoculation. However, inoculation with a mutant in the T3SS effector pth G reduced the expression of PIN2 by two‐fold compared with wild‐type infection. The results suggest that pth G might govern the elevation of PIN2 expression during infection, and that polar auxin transport‐derived IAA is essential for gall initiation.