Anti-LAMP2 Monoclonal antibody, clone BCM-04 [FITC]

The complex of Vacuolar Protein Sorting 34 and 15 (Vps34 and Vps15) has Class III phosphatidylinositol 3-kinase activity and putative roles in nutrient sensing, mammalian Target Of Rapamycin (mTOR) activation by amino acids, cell growth, vesicular trafficking and autophagy. Contrary to expectations, here we show that Vps15-deficient mouse tissues are competent for LC3-positive autophagosome formation and maintain mTOR activation. However, an impaired lysosomal function in mutant cells is traced by accumulation of adaptor protein p62, LC3 and Lamp2 positive vesicles, which can be reverted to normal levels after ectopic overexpression of Vps15. Mice lacking Vps15 in skeletal muscles, develop a severe myopathy. Distinct from the autophagy deficient Atg7-/- mutants, pathognomonic morphological hallmarks of autophagic vacuolar myopathy (AVM) are observed in Vps15-/- mutants, including elevated creatine kinase plasma levels, accumulation of autophagosomes, glycogen and sarcolemmal features within the fibres. Importantly, Vps34/Vps15 overexpression in myoblasts of Danon AVM disease patients alleviates the glycogen accumulation. Thus, the activity of the Vps34/Vps15 complex is critical in disease conditions such as AVMs, and possibly a variety of other lysosomal storage diseases.

Citrinin (CTN) is a secondary fungal metabolite produced by several species of Aspergillins and Penicillins, and it is widely found in vegetable-derived foods such as cereals and fermented rice-based food supplements. Previous studies indicated that CTN had immunotoxicity, hepatotoxicity, nephrotoxicity, and reproductive toxicity, which caused severe effects on human and animal health. However, the potential toxicity of CTN on the organelles of mouse oocytes is still unclear. In this study, we showed that the exposure to 30 mu M CTN significantly reduced the developmental capacity of mouse oocytes. Our results revealed that mitochondria exhibited abnormal distribution and mitochondrial membrane potential decreased under CTN exposure. And the endoplasmic reticulum (ER) failed to accumulate to the spindle periphery, which is accompanied by the occurrence of ER stress, showing with increased GRP78 expression. We also found that similar with ER, the Golgi apparatus showed homogenous localization pattern after CTN exposure, and the vesicle transport was disturbed, showing with aberrant expression and localization of Rab11a. Moreover, our results indicated that CTN exposure increased the expression of LAMP2, indicating the induction of lysosomal damage. In summary, our study showed that CTN exposure to mouse oocytes was toxic to the distribution and functions of organelles, which further led to a decrease of oocyte quality.