The Arabidopsis aberrant growth and death2 mutant shows resistance to Pseudomonas syringae and reveals a role for NPR1 in suppressing hypersensitive cell death

Citation
Dn. Rate et Jt. Greenberg, The Arabidopsis aberrant growth and death2 mutant shows resistance to Pseudomonas syringae and reveals a role for NPR1 in suppressing hypersensitive cell death, PLANT J, 27(3), 2001, pp. 203-211
Citations number
34
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Plant Sciences","Animal & Plant Sciences
Journal title
PLANT JOURNAL
ISSN journal
0960-7412 → ACNP
Volume
27
Issue
3
Year of publication
2001
Pages
203 - 211
Database
ISI
SICI code
0960-7412(200108)27:3<203:TAAGAD>2.0.ZU;2-8
Abstract
A novel Arabidopsis mutant has been identified with constitutive expression of GST1-GUS using plants with a pathogen-responsive reporter transgene con taining the beta -glucuronidase (GUS) coding region driven by the GST1 prom oter. The recessive mutant, called agd2 (aberrant growth and death2), has s alicylic acid (SA)-dependent increased resistance to virulent and avirulent strains of the bacterial pathogen Pseudomonas syringae, elevated SA levels , a low level of spontaneous cell death, callose deposition, and enlarged c ells in leaves. The enhanced resistance of agd2 to virulent P. syringae req uires the SA signaling component NONEXPRESSOR OF PR1 (NPR1). However, agd2 renders the resistance response to P. syringae carrying avrRpt2 NPR1-indepe ndent. Thus agd2 affects both an SA- and NPR1-dependent general defense pat hway and an SA-dependent, NPR1-independent pathway that is active during th e recognition of avirulent P. syringae. agd2 plants also fail to show a hyp ersensitive cell death response (HR) unless NPR1 is removed. This novel fun ction for NPR1 is also apparent in otherwise wild-type plants: npr1 mutants show a stronger HR, while NPR1-overproducing plants show a weaker HR when infected with P. syringae carrying the avrRpm1 gene. Spontaneous cell death in agd2 is partially suppressed by npr1, indicating that NPR1 can suppress or enhance cell death depending on the cellular context. agd2 plants deple ted of SA show a dramatic exacerbation of the cell-growth phenotype and inc reased callose deposition, suggesting a role for SA in regulating growth an d this cell-wall modification. AGD2 may function in cell death and/or growt h control as well as the defense response, similarly to what has been descr ibed in animals for the functions of NF kappaB.