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
Comparative Study
. 1992 Jan;11(1):87-96.
doi: 10.1002/j.1460-2075.1992.tb05031.x.

GAC1 may encode a regulatory subunit for protein phosphatase type 1 in Saccharomyces cerevisiae

Affiliations
Comparative Study

GAC1 may encode a regulatory subunit for protein phosphatase type 1 in Saccharomyces cerevisiae

J M François et al. EMBO J. 1992 Jan.

Abstract

Elevated dosage of the GAC1 gene from the yeast Saccharomyces cerevisiae causes hyperaccumulation of glycogen whereas a gene disruption of GAC1 results in reduced glycogen levels. Glycogen synthase is almost entirely in the active, glucose 6-phosphate-independent, form in cells with increased gene dosage of GAC1 whereas the enzyme is mostly in the inactive form in strains lacking GAC1. GAC1 encodes an 88 kDa protein that is similar to the regulatory subunit (RG1) of phosphoprotein phosphatase type 1 (PP-1) from skeletal muscle that targets PP-1 to glycogen particles. Taken together, these results suggest that GAC1 encodes a regulatory subunit of PP-1. As previously shown for glycogen phosphorylase (GPH1), GAC1 RNA accumulates concomitantly with the appearance of glycogen. A strain with a mutation in the regulatory subunit of the cAMP-dependent protein kinase (bcy1) fails to accumulate GPH1 and GAC1 RNA. These results point to coordinate regulation of enzymes involved in glycogen metabolism at the level of RNA accumulation and indicate that at least part of this control is exerted by the RAS-cAMP pathway.

PubMed Disclaimer

References

    1. Cell. 1989 Jun 16;57(6):987-96 - PubMed
    1. Cell. 1989 Jun 16;57(6):1009-16 - PubMed
    1. Proc Natl Acad Sci U S A. 1989 Nov;86(22):8778-82 - PubMed
    1. J Biol Chem. 1989 Dec 25;264(36):21435-8 - PubMed
    1. Cell. 1989 Feb 10;56(3):409-19 - PubMed

Publication types