THE L-CYSTEINE DESULFHYDRASE 1 (DES1) IS REQUIRED FOR ABA-DEPENDENT STOMATAL CLOSURE

DENISE SCUFFI; CONSOLACIÓN ÁLVAREZ; LASPINA, NATALIA; CECILIA GOTOR; LORENZO LAMATTINA; CARLOS GARCIA-MATA

Mar del Plata

Congreso; XXIX Reunion Argentina de Fisiología Vegetal; 2012

Stomatal pore regulation is a key process for carbon and water homeostasis of terrestrial plants. Abscisic acid (ABA), the most studied regulator of stomatal movement, induces stomatal closure through volume changes of stomatal guard cells. Hydrogen sulfide (H2S) has recently emerged as a new component of ABA signaling network in guard cells. H2S, is a small gas considered as the third endogenous gaseous transmitter in both in animals and plants. In Arabidopsis, H2S is enzymatically produced in the cytosol by the L-cysteine desulfhydrase DES1. In our lab we have recently showed that H2S induces stomatal closure in different plant species. Stomatal aperture experiments indicate that knock out mutant plants of DES1 gene are impaired to close the stomata in response to ABA. In the present work we studied the expression and activity of DES1 and its participation in ABA-dependent stomatal closure. qRT-PCR analysis showed that ABA induces DES1 expression in guard cell enriched extracts (GC-e) but not in mesophyll cell-enriched extracts (MC-e). This increase in DES1 expression upon ABA treatment is correlated with an increase of DES1 activity. Moreover, DES1 participation in this process was further supported by the analysis of the expression of ABA response marker genes RD29A and Rab18 genes. RT-PCR experiments showed that ABA induces the expression of both RD29A and Rab18 in GC-e extracts from wild type plants but not in GC-e extracts from des1 plants. In addition we show that in planta des1 mutants have reduced sensitivity to ABA. The data presented in this work show in wild type plantas ABA treatment produces a significant reduction of stomatal conductance but that response is partially blocked in des1 mutants. All together, the presented data strongly support DES1 as a novel component of the ABA-dependent signaling in Arabidopsis guard cells.