Murine phosphatidylserine-specific phospholipase A1 (Ps-pla1) maps to Chromosome 16 but is distinct from the lpd (lipid defect) locus

Xiao Yan Wen, A. Keith Stewart, Jennifer Skaug, Ellen Wei, Lap Chee Tsui

Research output: Contribution to journalArticle

9 Scopus citations

Abstract

We have previously generated a mouse transgenic line with an insertional mutation designated lpd that demonstrates a phenotype of hypertriglyceridemia and fatty liver. Since the recently identified phosphatidylserine-specific phospholipase A1 (PS-PLA1) demonstrates significant homology to triglyceride lipases, we reasoned that the mouse Ps-pla1 gene may be the disrupted gene within the lpd locus. Using a rat PS-PLA1 cDNA sequence to search the EST database, we identified a mouse EST homolog AA839424. Sequencing analysis of AA839424 revealed a putative Ps-pla1 protein of 456 amino acids with extensive overall structural conservation with human and rat PS-PLA1 and with triglyceride lipases. Conserved sequences in Ps-pla1 include a lipase consensus sequences G×S×G, a catalytic triad, and eight of the ten conserved cysteine residues that are required for tertiary structure. Mouse Ps-pla1 carries a phosphatidylserine-binding motif that is absent in all triglyceride lipases. Using a mouse whole-genome radiation hybrid (WG-RH) mapping panel (T31), we mapped mouse Ps-pla1 to Chromosome (Chr) 16 between genetic markers D16Mit194 and D16Mit38, which is 17.1 cM centromeric to the lpd locus. On the basis of chromosome location, we conclude that Ps-pla1 and lpd are distinct genes in lipid metabolism.

Original languageEnglish (US)
Pages (from-to)129-132
Number of pages4
JournalMammalian Genome
Volume12
Issue number2
DOIs
StatePublished - Feb 22 2001

ASJC Scopus subject areas

  • Genetics

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