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Title: Arabidopsis suppressor mutant of abh1 shows a new face of the already known players : ABH1 (CBP80) and ABI4-in response to ABA and abiotic stresses during seed germination
Authors: Daszkowska-Golec, Agata
Wojnar, W.
Rosikiewicz, M.
Szarejko, Iwona
Małuszyński, Mirosław
Szweykowska-Kulińska, Z.
Jarmołowski, A.
Keywords: Abscisic Acid; Arabidopsis; seed dormancy
Issue Date: 2013
Citation: Plant Molecular Biology, Vol. 81, iss. 1-2 (2013), s. 189-209
Abstract: Although the importance of abscisic acid (ABA) in plant development and response to abiotic and biotic stresses is well recognized, the molecular basis of the signaling pathway has not been fully elucidated. Mutants in genes related to ABA are widely used as a tool for gaining insight into the mechanisms of ABA signal transduction and ABA-dependent stress response. We used a genetic approach of a suppressor screening in order to decipher the interaction between ABH1 (CBP80) and other components of ABA signaling. ABH1 (CBP80) encodes a large subunit of CBC (CAP BINDING COMPLEX) and the abh1 mutant is drought-tolerant and hypersensitive to ABA during seed germination. The suppressor mutants of abh1 were generated after chemical mutagenesis. The mutant named soa1 (suppressor of abh1 hypersensitivity to ABA 1) displayed an ABA-insensitive phenotype during seed germination. The genetic analysis showed that the soa1 phenotype is dominant in relation to abh1 and segregates as a single locus. Based on soa1's response to a wide spectrum of physiological assays during different stages of development, we used the candidate-genes approach in order to identify a suppressor gene. The molecular analysis revealed that mutation causing the phenotype of soa1 occurred in the ABI4 (ABA insensitive 4) gene. Analysis of pre-miR159 expression, whose processing depends on CBC, as well as targets of miR159: MYB33 and MYB101, which are positive regulators of ABA signaling, revealed a possible link between CBP80 (ABH1) and ABI4 presented here.
DOI: 10.1007/s11103-012-9991-1
ISSN: 0167-4412
Appears in Collections:Artykuły (WNP)

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