ABSTRACT
The mechanism of endoplasmic reticulum (ER)-Golgi complex (GC) traffic is conserved from yeast to higher animals, but the architectures and the dynamics of vesicles' traffic between ER and GC vary across cell types and species. Skeletal muscle is a unique tissue in which ER and GC undergo a structural reorganization during differentiation that completely remodels the secretory pathway. In mature skeletal muscle, the ER is turned into sarcoplasmic reticulum, which is composed of junctional and longitudinal regions specialized, respectively, in calcium release and uptake during contraction. During skeletal muscle differentiation, GC acquires a particular fragmented organization as it appears as spots both at the nuclear poles and along the fibers. The ubiquitary-expressed Yip1A isoform has been proposed to be involved in anterograde trafficking from the ER exit sites to the cis-side of the GC and in ER and GC architecture organization. We investigated the role of Yip1 in skeletal muscle. Here we report that, following skeletal muscle development, the expression of the Yip1A decreases and is replaced by the muscle-specific Yip1B isoform. Confocal microscope analysis revealed that in adult skeletal muscle the Yip1B isoform is localized in the ER-Golgi intermediate and cis-Golgi compartments. Finally, skeletal muscle knockdown experiments in vitro and in vivo suggested that Yip1B is not involved in GC structure maintenance.
Subject(s)
Endoplasmic Reticulum/chemistry , Golgi Apparatus/chemistry , Muscle, Skeletal/chemistry , Vesicular Transport Proteins/analysis , Vesicular Transport Proteins/metabolism , Animals , Cells, Cultured , Endoplasmic Reticulum/metabolism , Golgi Apparatus/metabolism , Mice , Muscle, Skeletal/metabolism , Protein Isoforms/analysis , Protein Isoforms/biosynthesis , Protein Isoforms/metabolism , Vesicular Transport Proteins/biosynthesisABSTRACT
Gastric cancer (GC) shows a familiar predisposition which is largely unexplained. In this study the hypothesis that radiation sensitivity is implicated in the familiar predisposition to GC was investigated by means of the cytokinesis-block micronucleus assay. Data indicate that a family history of GC is not associated with any of the biomarkers investigated and does not interact with the demographic variables considered. When study subjects were dichotomized around the median age, a significant prevalence of micronuclei was observed in older subjects. Age and both spontaneous and radiation-induced micronuclei were linearly correlated. The effect of age was not modified by gender or smoking habits.
