Display Settings:

Format

Send to:

Choose Destination
Plant Mol Biol. 2013 May;82(1-2):113-29. doi: 10.1007/s11103-013-0040-5. Epub 2013 Mar 13.

GmNFYA3, a target gene of miR169, is a positive regulator of plant tolerance to drought stress.

Author information

  • 1The National Key Facility for Crop Gene Resources and Genetic Improvement, Institute of Crop Science, Chinese Academy of Agricultural Sciences, Beijing 100081, China.

Abstract

Nuclear factor Y (NF-Y) is a heterotrimeric transcription factor composed of NF-YA, NF-YB and NF-YC proteins. In this study, we identified and characterized a gene, GmNFYA3, which encodes the NF-YA subunit of the NF-Y complex in soybeans (Glycine max L.). Real time RT-PCR analysis indicated that GmNFYA3 was induced by abscisic acid (ABA) and abiotic stresses, such as polyethylene glycol, NaCl and cold. Subcellular localization analysis suggested that GmNFYA3 may activate its specific targets in the nucleus. Histochemical β-glucuronidase (GUS) staining revealed that the expression of the GUS gene driven by the GmNFYA3 promoter occurred in various transgenic Arabidopsis tissues. Coexpression in Nicotiana benthamiana and 5' RACE assays indicated that miR169 directs GmNFYA3 mRNA cleavage in vivo. Overexpression of GmNFYA3 resulted in Arabidopsis with reduced leaf water loss and enhanced drought tolerance. In addition, the transgenic Arabidopsis exhibited increased sensitivity to high salinity and exogenous ABA. Moreover, the transcript levels of ABA biosynthesis (ABA1, ABA2), ABA signaling (ABI1, ABI2) and stress-responsive genes, including RD29A and CBF3, were generally higher in GmNFYA3 plants than in wild-type controls under normal conditions. These results suggest that the GmNFYA3 gene functions in positive modulation of drought stress tolerance and has potential applications in molecular breeding to enhance drought tolerance in crops.

PMID:
23483290
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Springer
    Loading ...
    Write to the Help Desk