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The Arabidopsis thaliana T-DNA insertion mutant rh57-1 exhibited hypersensitivity to glucose (Glc) and abscisic acid (ABA). The other two rh57 mutants also showed Glc hypersensitivity similar to rh57-1, strongly suggesting that the Glc-hypersensitive feature of these mutants results from mutation of AtRH57. rh57-1 and rh57-3 displayed severely impaired seedling growth when grown in Glc concentrations higher than 3%. The gene, AtRH57 (At3g09720), was expressed in all Arabidopsis organs and its transcript was significantly induced by ABA, high Glc and salt. The new AtRH57 belongs to class II DEAD-box RNA helicase gene family. Transient expression of AtRH57-EGFP (enhanced green fluorescent protein) in onion cells indicated that AtRH57 was localized in the nucleus and nucleolus. Purified AtRH57-His protein was shown to unwind double-stranded RNA independent of ATP in vitro. The ABA biosynthesis inhibitor fluridone profoundly redeemed seedling growth arrest mediated by sugar. rh57-1 showed increased ABA levels when exposed to high Glc. Quantitative real time polymerase chain reaction analysis showed that AtRH57 acts in a signaling network downstream of HXK1. A feedback inhibition of ABA accumulation mediated by AtRH57 exists within the sugar-mediated ABA signaling. AtRH57 mutation and high Glc conditions additively caused a severe defect in small ribosomal subunit formation. The accumulation of abnormal pre-rRNA and resistance to protein synthesis-related antibiotics were observed in rh57 mutants and in the wild-type Col-0 under high Glc conditions. These results suggested that AtRH57 plays an important role in rRNA biogenesis in Arabidopsis and participates in response to sugar involving Glc- and ABA signaling during germination and seedling growth.

The Arabidopsis thaliana T- DNA insertion mutant rh57-1 exhibited hypersensitivity to glucose ( Glc) and abscisic acid ( ABA). The other two rh57 mutants also showed Glc hypersensitivity similar to rh57-1, strongly suggesting that the Glc-hypersensitive feature of these mutants results from mutation of At RH57. rh57-1 and rh57-3 displayed severely impaired seedling growth when grown in Glc concentrations higher than 3%. The gene, At RH57 ( At3g09720), was expressed in all Arabidopsis organs and its transcript was significantly induced by ABA, high Glc and salt. The new At RH57 belongs to class II DEAD-box RNA helicase gene family. Transient expression of At RH57- EGFP (enhanced green fluorescent protein) in onion cells indicated that At RH57 was localized in the nucleus and nucleolus. Purified At RH57- His protein was shown to unwind double-stranded RNA independent of ATP in vitro. The ABA biosynthesis inhibitor fluridone profoundly redeemed seedling growth arrest mediated by sugar. rh57-1 showed increased ABA levels when exposed to high Glc. Quantitative real time polymerase chain reaction analysis showed that At RH57 acts in a signaling network downstream of HXK1. A feedback inhibition of ABA accumulation mediated by At RH57 exists within the sugar-mediated ABA signaling. At RH57 mutation and high Glc conditions additively caused a severe defect in small ribosomal subunit formation. The accumulation of abnormal pre-r RNA and resistance to protein synthesis-related antibiotics were observed in rh57 mutants and in the wild-type Col-0 under high Glc conditions. These results suggested that At RH57 plays an important role in r RNA biogenesis in Arabidopsis and participates in response to sugar involving Glc- and ABA signaling during germination and seedling growth. [ABSTRACT FROM AUTHOR]

• gsm1 was isolated from an Arabidopsis glucose-hypersensitive mutant screen. • GSM1 encodes a putative RNA helicase and was localized to the nucleus. • gsm1 was sensitive not only to glucose but also to ABA. • GSM1 negatively regulates Glc-induced ABA signaling. In plants, sugar acts as an essential signaling molecule that modulates various aspects of metabolism, growth and development, which are also controlled by phytohormones. However, the molecular mechanism of cross-talk between sugar and phytohormones still remains to be elucidated. We have identified gsm1 (glucose-hypersensitive mutant 1) as a mutant with impaired cotyledon development that shows sensitivity to exogenous abscisic acid (ABA). The addition of fluridone can reverse the glucose (Glc) inhibitory effect in gsm1 , implying that endogenous ABA is involved in the Glc response of gsm1. In 4.5% Glc, the expression of Glc-induced ABA-responsive genes in gsm1-1 was nearly two times higher than that in the wild type. Compared to gsm1-1 , the gsm1-1 abi4-1 double mutant exhibited reduced sensitivity to Glc and ABA, which was similar to the Glc and ABA insensitive phenotype of abi4-1 , suggesting that ABI4 is epistatic to GSM1. In the treatment with 4.5% Glc, the GSM1 transcript level was greatly increased in abi4-1 by almost 4-fold of that in the wild type. These data suggest that GSM1 plays an important role in the ABI4-regulated Glc-ABA signaling cascade during Arabidopsis early seedling growth. [ABSTRACT FROM AUTHOR]