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Resistance to Botrytis cinerea Induced in Arabidopsis by Elicitors Is Independent of Salicylic Acid, Ethylene,

Summary: Resistance to Botrytis cinerea Induced in Arabidopsis by
Elicitors Is Independent of Salicylic Acid, Ethylene,
or Jasmonate Signaling But Requires
Simone Ferrari*, Roberta Galletti, Carine Denoux, Giulia De Lorenzo,
Frederick M. Ausubel, and Julia Dewdney
Dipartimento Territorio e Sistemi Agro-Forestali, Universita` degli Studi di Padova, 2335020 Legnaro, Italy
(S.F.); Department of Genetics, Harvard Medical School, and Department of Molecular Biology, Massachusetts
General Hospital, Boston, Massachusetts 02114 (C.D., F.M.A., J.D.); and Dipartimento di Biologia Vegetale,
Universita` di Roma La Sapienza, 00185 Rome, Italy (R.G., G.D.L.)
Oligogalacturonides (OGs) released from plant cell walls by pathogen polygalacturonases induce a variety of host defense
responses. Here we show that in Arabidopsis (Arabidopsis thaliana), OGs increase resistance to the necrotrophic fungal
pathogen Botrytis cinerea independently of jasmonate (JA)-, salicylic acid (SA)-, and ethylene (ET)-mediated signaling.
Microarray analysis showed that about 50% of the genes regulated by OGs, including genes encoding enzymes involved in
secondary metabolism, show a similar change of expression during B. cinerea infection. In particular, expression of
PHYTOALEXIN DEFICIENT3 (PAD3) is strongly up-regulated by both OGs and infection independently of SA, JA, and ET.
OG treatments do not enhance resistance to B. cinerea in the pad3 mutant or in underinducer after pathogen and stress1, a mutant
with severely impaired PAD3 expression in response to OGs. Similarly to OGs, the bacterial flagellin peptide elicitor flg22 also
enhanced resistance to B. cinerea in a PAD3-dependent manner, independently of SA, JA, and ET. This work suggests, therefore,
that elicitors released from the cell wall during pathogen infection contribute to basal resistance against fungal pathogens


Source: Ausubel, Frederick M. - Department of Genetics, Harvard University


Collections: Biology and Medicine