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Mapping MKP-3/FOXO1 interaction and evaluating the effect on gluconeogenesis.

Ping Jiao¹, Bin Feng, Haiyan Xu

¹Hallett Center for Diabetes and Endocrinology, Rhode Island Hospital, Alpert Medical School of Brown University, Providence, Rhode Island, United States of America.

|August 1, 2012

Summary

MAP kinase phosphatase 3 (MKP-3) activates FOXO1 to promote glucose production. This study identified key interaction sites and found MKP-3’s phosphatase activity is crucial for this process, impacting blood glucose levels.

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Area of Science:

Molecular Biology
Cellular Metabolism
Endocrinology

Background:

MAP kinase phosphatase 3 (MKP-3) regulates the ERK pathway and hepatic glucose production.
MKP-3 interacts with FOXO1 to promote glucose output, particularly in obesity.
Reduced hepatic MKP-3 expression lowers blood glucose in obese mouse models.

Purpose of the Study:

Investigate the mechanism of MKP-3/FOXO1 interaction.
Elucidate the effects on gluconeogenic gene transcription and glucose output.
Identify critical residues for MKP-3/FOXO1 interaction and functional consequences.

Main Methods:

Utilized mutated MKP-3 and FOXO1 adenoviral constructs in Fao hepatoma cells.
Assessed G6Pase gene expression changes with wild-type and inactive MKP-3.

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Published on: May 16, 2021

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Employed in vivo experiments with MKP-3 knockdown and FOXO1 mutants in mice.

Main Results:

MKP-3/FOXO1 interaction does not require MKP-3 phosphatase activity but is essential for FOXO1 nuclear translocation and gluconeogenesis.
MKP-3 significantly increased G6Pase gene expression, while inactive MKP-3 did not.
Specific residues (MKP-3: 200-260, FOXO1: 360-456) are critical for interaction.
ERK phosphorylation deficient FOXO1 mutant lost interaction with MKP-3.
Akt phosphorylation resistant FOXO1 mutant rescued hypoglycemia induced by MKP-3 knockdown.

Conclusions:

Identified critical residues mediating MKP-3/FOXO1 interaction.
ERK and Akt phosphorylation pathways differentially affect FOXO1 interaction and activation.
Active FOXO1 can counteract the hypoglycemic effects of reduced hepatic MKP-3 expression.