Abstract:
:Invadolysin is a novel metalloprotease conserved amongst metazoans that is essential for life in Drosophila. We previously showed that invadolysin was essential for the cell cycle and cell migration, linking to metabolism through a role in lipid storage and interaction with mitochondrial proteins. In this study we demonstrate that invadolysin mutants exhibit increased autophagy and decreased glycogen storage - suggestive of a role for invadolysin in insulin signaling in Drosophila. Consistent with this, effectors of insulin signaling were decreased in invadolysin mutants. In addition, we discovered that invadolysin was deposited on newly synthesized lipid droplets in a PKC-dependent manner. We examined two in vitro models of adipogenesis for the expression and localization of invadolysin. The level of invadolysin increased during both murine 3T3-L1 and human Simpson-Golabi-Behmel syndrome (SGBS), adipogenesis. Invadolysin displayed a dynamic localization to lipid droplets over the course of adipogenesis, which may be due to the differential expression of distinct invadolysin variants. Pharmacological inhibition of adipogenesis abrogated the increase in invadolysin. In summary, our results on in vivo and in vitro systems highlight an important role for invadolysin in insulin signaling and adipogenesis.
journal_name
Biol Chemjournal_title
Biological chemistryauthors
Chang CW,Abhinav K,Di Cara F,Panagakou I,Vass S,Heck MMdoi
10.1515/hsz-2016-0226subject
Has Abstractpub_date
2017-03-01 00:00:00pages
373-393issue
3eissn
1431-6730issn
1437-4315pii
/j/bchm.2017.398.issue-3/hsz-2016-0226/hsz-2016-02journal_volume
398pub_type
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