Sheng-Wen Chen
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Sheng-Wen Chen has a total of 8 co-authors. Here are the top co-authors by number of shared publications:
- Andy Golden
Laboratory of Biochemistry and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA
1 shared publication - Ben Nebenfuehr
Molecular, Cellular and Developmental Biology, University of Colorado, Boulder, Boulder, CO, USA
1 shared publication - Brian Wysolmerski
Department of Biology and Program in Molecular Biology, Pomona College, Claremont, CA
1 shared publication - Chao-Wen Wang
Department of Life Sciences, National Cheng Kung University, Tainan, Taiwan
1 shared publication - Jui-Ching Wu
Department of Clinical Laboratory Science and Medical Biotechnology, College of Medicine, National Taiwan University , Taipei 100229
1 shared publication - Leng-Jie Huang
Institute of Plant and Microbial Biology, Academia Sinica, Nankang, Taipei, Taiwan
1 shared publication
Latest Publications
- Open Access
- 23 January 2020
- Published by Cold Spring Harbor Laboratory in bioRxiv
Dietary supplementation with PUFAs rescues the eggshell defects caused byseipinmutations inC. elegans
SEIPIN, an ER membrane protein, plays critical roles in lipid droplet (LD) formation and lipid storage. Dysfunction of SEIPIN causes a variety of human diseases, including lipodystrophy, neuropathies, and male and female infertility. However, the cellular and molecular mechanisms of SEIPIN in causing these diseases are poorly understood. To address such mechanisms, we investigated the functional roles ofR01B10.6 (seip-1), the soleSEIPIN1ortholog inC. elegans,using CRISPR/Cas9 gene editing, and transcriptional assays. SEIP-1::mScarlet is widely expressed throughout development inC. elegans. Three full gene deletion mutants, generated by CRISPR/Cas9, displayed penetrant embryonic lethality. EM imaging and the visualization of reporter genes revealed that the lipid-rich permeability barrier, the innermost layer of theC. elegansembryonic eggshell, was defective or missing. Intriguingly, depletion of SEIP-1 revealed a perturbed gene expression pattern for fatty acid biosynthesis enzymes, in agreement with the disrupted permeability barrier formation phenotype of the embryos. Lastly, dietary supplementation of PUFAs rescued the embryonic lethality and defective permeability barrier in the deletion mutants. In sum, our study suggests that SEIP-1 may maternally regulate LD biogenesis and maintain lipid homeostasis to orchestrate the formation of the lipid-rich permeability barrier, which is crucial for eggshell formation and embryogenesis.
- 23 January 2020
- Published by Cold Spring Harbor Laboratory in bioRxiv
Open AccessDietary supplementation with PUFAs rescues the eggshell defects caused byseipinmutations inC. elegans
SEIPIN, an ER membrane protein, plays critical roles in lipid droplet (LD) formation and lipid storage. Dysfunction of SEIPIN causes a variety of human diseases, including lipodystrophy, neuropathies, and male and female infertility. However, the cellular and molecular mechanisms of SEIPIN in causing these diseases are poorly understood. To address such mechanisms, we investigated the functional roles ofR01B10.6 (seip-1), the soleSEIPIN1ortholog inC. elegans,using CRISPR/Cas9 gene editing, and transcriptional assays. SEIP-1::mScarlet is widely expressed throughout development inC. elegans. Three full gene deletion mutants, generated by CRISPR/Cas9, displayed penetrant embryonic lethality. EM imaging and the visualization of reporter genes revealed that the lipid-rich permeability barrier, the innermost layer of theC. elegansembryonic eggshell, was defective or missing. Intriguingly, depletion of SEIP-1 revealed a perturbed gene expression pattern for fatty acid biosynthesis enzymes, in agreement with the disrupted permeability barrier formation phenotype of the embryos. Lastly, dietary supplementation of PUFAs rescued the embryonic lethality and defective permeability barrier in the deletion mutants. In sum, our study suggests that SEIP-1 may maternally regulate LD biogenesis and maintain lipid homeostasis to orchestrate the formation of the lipid-rich permeability barrier, which is crucial for eggshell formation and embryogenesis.