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Atypical mannolipids characterize Thy-1-negative lymphoma mutants.
P Lemansky1, D K Gupta, S Meyale
1Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106.
Molecular and Cellular Biology
|August 1, 1991
Summary
Murine lymphoma cells deficient in complete mannolipids fail to express surface proteins like Thy-1. This suggests mannolipid anchor defects may underlie paroxysmal nocturnal hemoglobinuria.
Area of Science:
- Cell Biology
- Biochemistry
Background:
- Eukaryotic cells, including murine lymphomas, express surface proteins anchored by phosphoinositol mannolipids.
- Thy-1 is an example of a surface protein with a mannolipid anchor.
Purpose of the Study:
- To investigate the role of mannolipid anchors in protein expression.
- To identify defects in mannolipid biosynthesis in lymphoma mutants.
- To explore potential links between mannolipid anchor defects and human diseases like paroxysmal nocturnal hemoglobinuria.
Main Methods:
- Analysis of Thy-1-negative lymphoma mutants.
- Detection of mannolipid anchor precursors.
- Structural analysis of mannolipids in wild-type and mutant cells.
Main Results:
- Six Thy-1-negative mutants lacked complete mannolipids.
- Three mutants synthesized atypical mannolipids.
- Absence of complete mannolipids correlated with lack of expression of multiple mannolipid-anchored proteins.
Conclusions:
- Defects in mannolipid anchor biosynthesis can explain the lack of surface protein expression in lymphoma mutants.
- Mannolipid anchor deficiencies may contribute to the pathogenesis of paroxysmal nocturnal hemoglobinuria.
- Anchor biosynthesis may involve intermediate transmembrane flip-flop and deacylation steps.