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Defining Substrate Specificities for Lipase and Phospholipase Candidates

Defining Substrate Specificities for Lipase and Phospholipase Candidates

Published on: November 23, 2016

Orm family proteins mediate sphingolipid homeostasis.

David K Breslow¹, Sean R Collins, Bernd Bodenmiller

¹Department of Cellular and Molecular Pharmacology, University of California, San Francisco, 1700 4th Street, San Francisco, California 94158, USA.

|February 26, 2010

Summary

Researchers discovered Orm proteins regulate sphingolipid synthesis. Phosphorylation controls this regulation, linking sphingolipid homeostasis to childhood asthma risk.

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Area of Science:

Cellular Biology
Biochemistry
Genetics

Background:

Sphingolipids are vital membrane components and signaling molecules.
Cellular regulation of sphingolipid levels remains poorly understood.
ORM genes, including human ORMDL3, are implicated in childhood asthma.

Purpose of the Study:

To elucidate the function of ORM genes in sphingolipid metabolism.
To identify the regulatory mechanisms controlling sphingolipid synthesis.
To explore the link between sphingolipid dysregulation and asthma.

Main Methods:

Functional genomic screening in Saccharomyces cerevisiae.
Biochemical assays to characterize protein interactions.
Analysis of gene expression and protein phosphorylation.

Main Results:

Orm proteins act as negative regulators of sphingolipid synthesis.
Orm proteins form a complex with serine palmitoyltransferase.
Phosphorylation of Orm proteins modulates their inhibitory activity.
ORM gene expression changes or phosphorylation site mutations disrupt sphingolipid homeostasis.

Conclusions:

Orm proteins are critical mediators of sphingolipid homeostasis.
Dysregulation of sphingolipid metabolism may contribute to childhood asthma.
This study reveals a novel regulatory pathway for sphingolipid synthesis.