Magic™ Anti-dynamin (Phospho S778) polyclonal antibody

Mig2 has been described as a transcriptional factor that in the absence of Mig1 protein is required for glucose repression of the SUC2 gene. Thus, until now, the main role assigned to Mig2 has been the functional redundancy to Mig1. in this study, we report that Mig2 has a double subcellular localization. As expected, in high-glucose conditions it is accumulated in the nucleus but in low-glucose conditions Mig2 has an unexpected mitochondrial localization and role in mitochondrial morphology. We describe that Mig2 physically interacts with the mitochondrial protein Ups1 in a glucose-dependent manner. We also show that Delta mig2 mutant cells exhibit a fragmented network of mitochondrial tubules, a phenotype similarly observed in cells lacking Fzo1 and Ups1. Furthermore, Mig2 acts antagonistically with respect to the fission-promoting components, because mitochondrial aggregation induced by DNM1 deletion was rescued in the Delta dnm1 Delta mig2 double mutant. Thus, our studies have revealed an additional role for Mig2 as a novel factor required for the maintenance of fusion-competent mitochondria in Saccharomyces cerevisiae and strongly suggest that Mig2 could be involved in the cross talk between the nucleus and the mitochondria through Ups1 to regulate mitochondrial morphology in a glucose dependent manner. (C) 2012 Elsevier B.V. and Mitochondria Research Society. All rights reserved.

PURPOSE. To determine whether elevation of intraocular pressure (IOP) triggers mitochondrial fission and ultrastructural changes and alters optic atrophy type 1 (OPA1) expression and distribution in the optic nerve (ON) of glaucomatous DBA/2J mice. METHODS. IOP in the eyes of DBA/2J mice was measured, and mitochondrial structural changes were assessed by conventional electron microscopy (EM) and EM tomography. Cytochrome c oxidase IV subunit 1 (COX), OPA1, and Dnm1, a rat homologue of dynamin-related protein-1, mRNA were measured by quantitative (q) PCR. COX and OPA1 protein distribution was assessed by immunocytochemistry and Western blot. RESULTS. Excavation of the optic nerve head (ONH), axon loss, and COX reduction were evident in 10-month-old glaucomatous ONHs of eyes with > 20 mm Hg IOP elevation. EM analysis showed mitochondrial fission, matrix swelling, substantially reduced cristae volume, and abnormal cristae depletion in 10-month-old glaucomatous ONH axons. The mean length of mitochondrial cross section in these axons decreased from 858.2 +/- 515.3 nm in 3-month-old mice to 583.3 +/- 298.6 nm in 10-month-old glaucomatous mice (P < 0.001). Moderate reductions of COX mRNA were observed in the 10-month-old DBA/2J mice's ONHs. Larger reductions of OPA1 immunoreactivity and gene expression were coupled with larger increases of Dnm1 gene expression in 10-month-old glaucomatous ONH. Subcellular fractionation analysis indicates increased release of both OPA1 and cytochrome c from mitochondria in 10-month-old glaucomatous ONs. CONCLUSIONS. IOP elevation may directly damage mitochondria in the ONH axons by promoting reduction of COX, mitochondrial fission and cristae depletion, alterations of OPA1 and Dnm1 expression, and induction of OPA1 release. Thus, interventions to preserve mitochondria may be useful for protecting against ON degeneration in glaucoma. (Invest Ophthalmol Vis Sci. 2008;49:4903-4911) DOI: 10.1167/iovs.07-1661