Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1998 Sep;15(5):685-95.
doi: 10.1046/j.1365-313x.1998.00244.x.

The 3' untranslated region of a rice alpha-amylase gene mediates sugar-dependent abundance of mRNA

Affiliations
Free article

The 3' untranslated region of a rice alpha-amylase gene mediates sugar-dependent abundance of mRNA

M T Chan et al. Plant J. 1998 Sep.
Free article

Abstract

A decrease in transcript stability is one of the important mechanisms that control the sugar repression of alpha-amylase gene expression in rice suspension cells. In this study, we investigated the function of the 3' untranslated region (3'UTR) of a rice alpha-amylase gene, alpha Amy3, in relation to sugar-dependent accumulation of mRNA. By examining the transient expression of chimeric genes in rice protoplasts, we were able to demonstrate that the alpha Amy3 3'UTR mediated the sugar-dependent repression of fused heterologous gene expression. The same kinetics of accumulation of alpha Amy3 mRNA and reporter mRNA carrying the alpha Amy3 3'UTR in response to glucose deprivation were observed, suggesting that the alpha Amy3 3'UTR is sufficient, and probably the major determinant for controlling the abundance of these transcripts. Functional analysis of two subdomains of alpha Amy3 3'UTR by insertion into a sugar-inducible chimeric gene confirmed their roles in sugar repressibility. The regulatory sequences in the alpha Amy3 3'UTR may act as potent determinants of mRNA stability in response to sugar availability. This finding has important implications for studying the regulatory mechanism of sugar repression in eukaryotes.

PubMed Disclaimer

Publication types

LinkOut - more resources