Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Multiple levels of tobacco WIPK activation during the induction of cell death by fungal elicitins
Autore:
Zhang, SQ; Liu, YD; Klessig, DF;
Indirizzi:
Rutgers State Univ, Waksman Inst, Piscataway, NJ 08854 USA Rutgers State Univ Piscataway NJ USA 08854 Inst, Piscataway, NJ 08854 USA Rutgers State Univ, Dept Mol Biol & Biochem, Piscataway, NJ 08854 USA Rutgers State Univ Piscataway NJ USA 08854 chem, Piscataway, NJ 08854 USA Univ Missouri, Dept Biochem, Columbia, MO 65211 USA Univ Missouri Columbia MO USA 65211 Dept Biochem, Columbia, MO 65211 USA
Titolo Testata:
PLANT JOURNAL
fascicolo: 3, volume: 23, anno: 2000,
pagine: 339 - 347
SICI:
0960-7412(200008)23:3<339:MLOTWA>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
RECEPTOR-MEDIATED ACTIVATION; PROTEIN-KINASE; SIGNAL-TRANSDUCTION; MAP KINASE; RESISTANCE GENE; PLANT-CELLS; TRANSIENT ACTIVATION; PATHOGEN DEFENSE; PHOSPHORYLATION; STRESS;
Keywords:
MAP kinases; WIPK; SIPK; elicitin; transcription; translation;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Agriculture,Biology & Environmental Sciences
Life Sciences
Citazioni:
44
Recensione:
Indirizzi per estratti:
Indirizzo: Klessig, DF Rutgers State Univ, Waksman Inst, 190 Frelinghuysen Rd, Piscataway, NJ 08854 USA Rutgers State Univ 190 Frelinghuysen Rd Piscataway NJ USA 08854
Citazione:
S.Q. Zhang et al., "Multiple levels of tobacco WIPK activation during the induction of cell death by fungal elicitins", PLANT J, 23(3), 2000, pp. 339-347

Abstract

Three protein kinases of 48, 44 and 40 kDa are activated at different stages in tobacco cells treated with fungal elicitins. Previously we demonstrated that the rapidly activated 48 kDa protein kinase is encoded by SIPK. Here we report that the elicitin-activated 44 kDa kinase is encoded by WIPK. Activation of this kinase occurred 2-4 h after elicitin treatment and was preceded by dramatic increases in WIPK mRNA and protein levels. Studies usingactinomycin D and cycloheximide demonstrated that de novo transcription and translation were required for this activation of the kinase activity. Strikingly, the kinetics of WIPK activation following elicitin treatment correlated with the onset of hypersensitive response (HR)-like cell death. Moreover, staurosporine and K-252a, two Ser/Thr protein kinase inhibitors that blocked WIPK activation, suppressed cell death. The timing for elicitin-treated cells to commit to a death program correlated with the appearance of high levels of WIPK activity. These correlative data suggest that WIPK may play a role during HR development in tobacco. Interestingly, a fungal cell-wall elicitor that does not cause cell death induced WIPK mRNA and protein tosimilar levels as those observed with the elicitins. However, no corresponding increase in WIPK activity was detected. Thus WIPK appears to be controlled at multiple levels.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/03/20 alle ore 22:53:33