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Nazo, the Drosophila homolog of the NBIA-mutated protein – c19orf12, is required for triglyceride homeostasis

View ORCID ProfilePerinthottathil Sreejith, Sara Lolo, Kristen R. Patten, Maduka Gunasinghe, Neya More, Leo J. Pallanck, View ORCID ProfileRajnish Bharadwaj
doi: https://doi.org/10.1101/2022.09.29.510106
Perinthottathil Sreejith
1Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY, USA
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  • ORCID record for Perinthottathil Sreejith
Sara Lolo
1Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY, USA
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Kristen R. Patten
1Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY, USA
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Maduka Gunasinghe
1Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY, USA
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Neya More
1Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY, USA
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Leo J. Pallanck
2Department of Genome Sciences, University of Washington, Seattle, WA, USA
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Rajnish Bharadwaj
1Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY, USA
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  • ORCID record for Rajnish Bharadwaj
  • For correspondence: Rajnish_bharadwaj@urmc.rochester.edu
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SUMMARY

Lipid dyshomeostasis has been implicated in a variety of diseases ranging from obesity to neurodegenerative disorders such as NBIA. Here, we uncover the physiological role of Nazo, the Drosophila homolog of the NBIA-mutated protein – c19orf12, whose function has been elusive. Ablation of Drosophila c19orf12 homologs leads to dysregulation of multiple lipid metabolism genes. nazo mutants exhibit markedly reduced gut lipid droplet and whole-body triglyceride contents. Consequently, they are sensitive to starvation and oxidative stress. Nazo localizes to ER-lipid droplet contact sites and is required for maintaining normal levels of Perilipin2, an inhibitor of the lipase – Brummer. Concurrent knockdown of Brummer or overexpression of Perilipin2 rescues the nazo phenotype, suggesting that this defect may arise from diminished Perilipin2 on lipid droplets leading to aberrant Brummer-mediated lipolysis. Our findings provide novel insights into the role of c19orf12 as a possible link between lipid dyshomeostasis and neurodegeneration, particularly in the context of NBIA.

Competing Interest Statement

The authors have declared no competing interest.

Copyright 
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license.
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Posted September 30, 2022.
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Nazo, the Drosophila homolog of the NBIA-mutated protein – c19orf12, is required for triglyceride homeostasis
Perinthottathil Sreejith, Sara Lolo, Kristen R. Patten, Maduka Gunasinghe, Neya More, Leo J. Pallanck, Rajnish Bharadwaj
bioRxiv 2022.09.29.510106; doi: https://doi.org/10.1101/2022.09.29.510106
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Nazo, the Drosophila homolog of the NBIA-mutated protein – c19orf12, is required for triglyceride homeostasis
Perinthottathil Sreejith, Sara Lolo, Kristen R. Patten, Maduka Gunasinghe, Neya More, Leo J. Pallanck, Rajnish Bharadwaj
bioRxiv 2022.09.29.510106; doi: https://doi.org/10.1101/2022.09.29.510106

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