PARTICIPATION OF EXTRACELLULAR NUCLEOTIDES IN THE WOUND RESPONSE OF DASYCLADUS VERMICULARIS AND ACETABULARIA ACETABULUM (DASYCLADALES, CHLOROPHYTA)(1)

© 2008 Phycological Society of America.

Détails bibliographiques
Publié dans:Journal of phycology. - 1966. - 44(2008), 6 vom: 04. Dez., Seite 1504-11
Auteur principal: Torres, Jonathan (Auteur)
Autres auteurs: Rivera, Amy, Clark, Greg, Roux, Stanley J
Format: Article en ligne
Langue:English
Publié: 2008
Accès à la collection:Journal of phycology
Sujets:Journal Article Acetabularia acetabulum Dasycladus vermicularis extracellular ATP hydrogen peroxide macroalgae nitric oxide purinoceptor antagonist wounding
Description
Résumé:© 2008 Phycological Society of America.
As assayed by fluorescent reporter dyes, nitric oxide (NO) and H2 O2 , two downstream signaling agents induced by wounding in the alga Dasycladus vermicularis (Scop.) Krasser, can also be induced in unwounded Dasycladus cells by μM Adenosine 5'[γ-thio]triphosphate (ATPγS) and Adenosine 5'-[β-thio]diphosphate (ADPβS), but not by Adenosine 5'-O-thiomonophosphate (AMPS). These nucleotide-induced responses are blocked by pyridoxalphosphate-6-azophenyl-2',4'-disulphonic acid (PPADS), an antagonist of animal purinoceptors, and by adenosine, a feed-back inhibitor of extracellular nucleotide responses in animals. Similar nucleotide- and nucleotide-antagonist responses were observed in Acetabularia acetabulum (L.) P. C. Silva. Significant levels of ATP released from Dasycladus cells were measured at wound sites by a sensitive luciferin-luciferase assay. Additionally, the normal wound-induced production of NO and H2 O2 in Dasycladus can be blocked by pretreating the cells with PPADS. Our results indicate that nucleotides released from wounds can serve as a signal to trigger wound responses in algae, and that coordinated signaling between extracellular nucleotides and the NO pathway may have been established early during the evolution of plants
Description:Date Completed 05.04.2016
Date Revised 04.04.2016
published: Print
Citation Status PubMed-not-MEDLINE
ISSN:1529-8817
DOI:10.1111/j.1529-8817.2008.00602.x