Interaction of serologically defined colon cancer antigen-3 with Arf6 and its predominant expression in the mouse testis

ADP ribosylation factor 6 (Arf6) is a small GTPase that regulates endosomal trafficking and actin cytoskeleton remodeling. Here, we identified the serologically defined colon antigen-3 (SDCCAG3) as an Arf6-interacting protein by yeast two-hybrid screening with a constitutively active Arf6 mutant. SD...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2016-09, Vol.477 (4), p.868-873
Main Authors: Sakagami, Hiroyuki, Hara, Yoshinobu, Fukaya, Masahiro
Format: Article
Language:English
Subjects:
ADP-Ribosylation Factors - metabolism
Animals
Antigens, Neoplasm
Antigens, Surface - metabolism
Carrier Proteins - metabolism
Cytokinesis
Endosome
Gene Expression Regulation - physiology
Male
Membrane trafficking
Mice
Mice, Inbred C57BL
Organ Specificity - physiology
Protein Binding
Small GTPase
Testis
Testis - metabolism
Tissue Distribution
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Summary:ADP ribosylation factor 6 (Arf6) is a small GTPase that regulates endosomal trafficking and actin cytoskeleton remodeling. Here, we identified the serologically defined colon antigen-3 (SDCCAG3) as an Arf6-interacting protein by yeast two-hybrid screening with a constitutively active Arf6 mutant. SDCCAG3 interacts specifically with Arf6 among the Arf family members through its 101  C-terminal amino acids. SDCCAG3 is expressed most intensely in the testis at the mRNA and protein levels. In the testis, SDCCAG3 is expressed in spermatocytes and spermatids. We also show that full-length SDCCAG3, but not a mutant lacking the ability to interact with Arf6, is recruited to the midbody during cytokinesis when expressed exogenously in HeLa cells. These findings suggest that SDCCAG3 might function in endosomal trafficking downstream of Arf6. •SDCCAG3 interacts specifically with a GTP-locked Arf6 mutant.•SDCCAG3 is expressed most intensely in the testis.•The midbody localization of SDCCAG3 depends on the interaction with Arf6.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2016.06.150