TABLE 2.
Phenotypes of altered seipin expression
| Organism/cell manipulation | Phenotypes | Reference(s) |
| Saccharomyces cerevisiae FLD1 disruption | Shorter and more-saturated acyl chains on phospholipids | Fei et al. 2008 |
| Increase in PA (isolated microsomes), TAG, and SE levels | Fei et al. 2008Fei et al. 2011 PLoS Gen | |
| No increase in oleate incorporation into TAG and SE; presumed decrease in lipid utilization | Fei et al. 2008 | |
| Upregulation of INO1 and OPI3 | Fei et al. 2011 PLoS Gen | |
| Small clustered LDs wrapped in ER | Szymanski et al. 2007 | |
| Enhanced LD fusion and supersized droplets (rescued by inositol supplementation) | Fei et al. 2008Fei et al. 2011 PLoS Gen | |
| Tgl3p mistargeting | Wolinski et al. 2011 | |
| LD segregation defect | Wolinski et al. 2011 | |
| Drosophila melanogaster seipin knockout | Fat body: less neutral lipid; small droplets; decreased lipogenesis | Tian et al. 2011 |
| Salivary gland and midgut: larger and more-numerous LDs; PA and DGAT elevated; phenotype suppressed by DGAT knockdown | ||
| Organism: hypersensitive to starvation; lower glucose tolerance | ||
| Mus musculusseipin knockout | Adipose tissue: decrease in WAT and BAT mass; small unilocular droplets | Cui et al. 2011 |
| Liver: enlarged; large increase in lipid storage | ||
| Organism: lower body weight at birth; higher temperature; decreased adipokines; diabetic; impaired insulin signaling | ||
| HeLa seipin knockdown | Increase in TAG, LD proliferation and clustering (with exogenous oleate) | Fei et al. 2011 JLR |
| HaLa seipinoverexpression | Reduction in TAG with no change in FA uptake or lipolysis (with exogenous oleate) | |
| Mouse 3T3-L1seipin knockdown | Block in terminal differentiation | Chen et al. 2009 |
| Increased TAG (with exogenous oleate) | Fei et al. 2011 JLR | |
| Mouse C3H 10T1/2 seipin knockdown | Block in terminal differentiation | Payne et al. 2008 |
| BSCL2 patient-derived cells | Fibroblasts: small numerous LDs | Szymanski et al. 2007 |
| Transformed lymphocytes: small numerous LDs; more-saturated FAs (presumed due to less SCD1 activity) | Boutet et al. 2009 |