INVESTIGADORES
GARCIA-MATA Carlos
artículos
Título:
Hydrogen sulfide generated by L-cysteine desulfhydrase acts upstream of nitric oxide to modulate ABA-dependent stomatal closure.
Autor/es:
DENISE SCUFFI; CONSOLACIÓN ÁLVAREZ; LASPINA, NATALIA; CECILIA GOTOR; LORENZO LAMATTINA; CARLOS GARCIA-MATA
Revista:
PLANT PHYSIOLOGY.
Editorial:
AMER SOC PLANT BIOLOGISTS
Referencias:
Lugar: Rockville; Año: 2014 vol. 166 p. 2065 - 2076
ISSN:
0032-0889
Resumen:
Abscisic acid (ABA) is a well-studied regulator of stomatal movement. Hydrogen sulfide (H2S), a small signaling gas molecule involved in key physiological processes in mammals, has been recently reported as a new component of ABA signaling network in stomatal guard cells. In Arabidopsis, H2S is enzymatically produced in the cytosol through the activity of L-cysteine desulfhydrase (DES1). In the present work, we used DES1 knock-out Arabidopsis mutant plants (des1) to study the participation of DES1 in the crosstalk between H2S and nitric oxide (NO) in the ABA-dependent signaling network in guard cells. The results show that ABA did not close the stomata in isolated epidermal strips of des1 mutants, effect that was restored by the application of exogenous H2S. qRT-PCR analysis demonstrated that ABA induces DES1 expression in guard cell-enriched RNA extracts from wild type Arabidopsis plants. Furthermore, stomata from isolated epidermal strips of Arabidopsis ABA receptor mutant pyr1/pyl1/pyl2/pyl4 close in response to exogenous H2S suggesting that this gasotransmitter is acting downstream, although acting independently of ABA receptor cannot be rule out with the present data.. However Arabidopsis clade-A PP2C mutant abi1-1 do not close the stomata when epidermal strips are treated with H2S suggesting that H2S required a functional ABI1. Further studies to unravel the cross-talk between H2S and NO indicate that: (i) H2S promotes NO production, (ii) DES1 is required for ABA-dependent NO production, and (iii) NO is downstream of H2S in ABA-induced stomatal closure. Altogether, data indicate that DES1 is a novel component of ABA signaling in guard cells.