Impact of orm knock out on lipids in yeast

It was impossible to associated all the reported lipid entities to lipidmaps and pubchem identifiers. Out of over 300 species only 100 were mapped to IDs. So, I decided to choose an alternative way. First, a chemical similarity network was constructed for different types of lipid classes (diamonds in the figure) later on individual lipid species is connected to these lipid. Other option could be to use fatty acids and degree of un-saturation to connected lipid entities.


The data underlying this figure are coming from a supplementary table from a paper http://www.nature.com/nature/journal/v463/n7284/full/nature08787.html

Orm family proteins mediate sphingolipid homeostasis


Abstract

Despite the essential roles of sphingolipids both as structural components of membranes and critical signalling molecules, we have a limited understanding of how cells sense and regulate their levels. Here we reveal the function in sphingolipid metabolism of the ORM genes (known as ORMDL genes in humans)—a conserved gene family that includes ORMDL3, which has recently been identified as a potential risk factor for childhood asthma. Starting from an unbiased functional genomic approach in Saccharomyces cerevisiae, we identify Orm proteins as negative regulators of sphingolipid synthesis that form a conserved complex with serine palmitoyltransferase, the first and rate-limiting enzyme in sphingolipid production. We also define a regulatory pathway in which phosphorylation of Orm proteins relieves their inhibitory activity when sphingolipid production is disrupted. Changes in ORM gene expression or mutations to their phosphorylation sites cause dysregulation of sphingolipid metabolism. Our work identifies the Orm proteins as critical mediators of sphingolipid homeostasis and raises the possibility that sphingolipid misregulation contributes to the development of childhood asthma.