StarD7 deficiency hinders cell motility through p-ERK1/2/Cx43 reduction

StarD7 belongs to START protein family involved in lipid traffic, metabolism, and signaling events. Its precursor, StarD7.I which is important for mitochondrial homeostasis, is processed to the StarD7.II isoform that lacks the mitochondrial targeting sequence and is mainly released to the cytosol. S...

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Published in:PloS one 2022-12, Vol.17 (12), p.e0279912-e0279912
Main Authors: Cruz Del Puerto, Mariano, Rojas, María Laura, Racca, Ana Cristina, Kourdova, Lucille Tihomirova, Miranda, Andrea Lis, Panzetta-Dutari, Graciela, Genti-Raimondi, Susana, Flores-Martín, Jésica Belén
Format: Article
Language:English
Subjects:
Analysis
Antibodies
Biology and Life Sciences
Carrier Proteins - metabolism
Cell adhesion & migration
Cell migration
Cell Movement - genetics
Connexin 43
Connexin 43 - genetics
Connexin 43 - metabolism
Cytosol
Ectopic expression
Experiments
Extracellular signal-regulated kinase
Golgi cells
Homeostasis
Infrared imaging systems
Integrin beta1 - genetics
Integrin beta1 - metabolism
Integrins
Laboratories
Lipid metabolism
Lipids
MAP Kinase Signaling System
Membrane proteins
Metabolism
Mitochondria
Morphology
Physiological aspects
Plasmids
Protein Isoforms - metabolism
Protein turnover
Proteins
Research and Analysis Methods
Wound healing
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Summary:StarD7 belongs to START protein family involved in lipid traffic, metabolism, and signaling events. Its precursor, StarD7.I which is important for mitochondrial homeostasis, is processed to the StarD7.II isoform that lacks the mitochondrial targeting sequence and is mainly released to the cytosol. StarD7 knockdown interferes with cell migration by an unknown mechanism. Here, we demonstrate that StarD7 silencing decreased connexin 43 (Cx43), integrin β1, and p-ERK1/2 expression in the non-tumoral migratory HTR-8/SVneo cells. StarD7-deficient cells exhibited Golgi disruption and reduced competence to reorient the microtubule-organizing center. The migratory capacity of StarD7-silenced cells was reestablished when Cx43 level was resettled, while p-ERK1/2 expression remained low. Importantly, ectopic expression of the StarD7.II isoform not only restored cell migration but also ERK1/2, Cx43, and integrin β1 expression. Thus, StarD7 is implicated in cell migration through an ERK1/2/Cx43 dependent mechanism but independent of the StarD7.I function in the mitochondria.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0279912