AtGRDP1 Gene Encoding a Glycine-Rich Domain Protein Is Involved in Germination and Responds to ABA Signalling

Aída Araceli Rodríguez-Hernández, María Azucena Ortega-Amaro, Pablo Delgado-Sánchez, Julio Salinas, Juan Francisco Jiménez-Bremont

Producción científica: Contribución a una revistaArtículorevisión exhaustiva

21 Citas (Scopus)

Resumen

Seed maturation and germination involve changes in gene expression, as well as physiological and metabolic events; however, much remains to be learned. In plants, abiotic stress affects germination, growth and development, significantly reducing productivity, and in some cases, causing plant death. AtGRDP1 is a novel protein that contains a short glycine-rich domain, a DUF1399 domain, and a putative RNP motif. Expression analysis showed that AtGRDP1 gene is modulated in response to NaCl, LiCl, mannitol, sorbitol, glucose, and exogenous ABA. In order to characterise the AtGRDP1 gene, null mutant and overerexpressing lines were obtained. The Atgrdp1-null mutant line showed an increased sensitivity to salt and osmotic stress in germination and cotyledon development, whereas 35S::AtGRDP1 overerexpressing lines resulted in increased tolerance to abiotic stress. Interestingly, 35S::AtGRDP1 overerexpressing lines showed resistance to ABA, resembling a well-known ABI phenotype, whereas the disruption of AtGRDP1 gene resulted in ABA hypersensitivity, mimicking the ABI3-overexpression phenotype. Furthermore, we analysed the ABI3 and ABI5 genes, which are central regulators in ABA signalling, in Atgrdp1-null mutant and 35S::AtGRDP1 overerexpressing lines. Under ABA treatments, Atgrdp1-null mutant seedlings showed higher ABI3 and ABI5 transcript levels, whereas in 35S::AtGRDP1 overexpressing line, the ABI3 and ABI5 transcripts were repressed. These results suggest that AtGRDP1 gene plays a regulatory role in ABA signalling and tolerance to abiotic stress.

Idioma originalInglés
Páginas (desde-hasta)1187-1202
Número de páginas16
PublicaciónPlant Molecular Biology Reporter
Volumen32
N.º6
DOI
EstadoPublicada - 29 oct. 2014
Publicado de forma externa

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