Rationale Mitochondria interact via actions of outer and inner membrane fusion proteins. The role of mitochondrial fusion on functioning of the heart, where mitochondria comprise ~30% of cardiomyocyte volume and their inter-myofilament spatial arrangement with other mitochondria is highly ordered, is unknown. Objective Model and analyze mitochondrial fusion defects in Drosophila melanogaster heart tubes with tincΔ4Gal4-directed expression of RNAi for Mitochondrial Assembly Regulatory Factor (MARF) and Optic atrophy 1 (Opa1). Methods and Results Live imaging analysis revealed that heart tube-specific knockdown of MARF or Opa1 increases mitochondrial morphometric heterogeneity and induces heart tube dilation with profound contractile impairment. Sarcoplasmic reticular structure was unaffected. Cardiomyocyte expression of human mitofusin (mfn) 1 or 2 rescued MARF RNAi cardiomyopathy, demonstrating functional homology between Drosophila MARF and human mitofusins. Suppressing mitochondrial fusion increased compensatory expression of nuclear-encoded mitochondrial genes, indicating mitochondrial biogenesis. The MARF RNAi cardiomyopathy was prevented by transgenic expression of superoxide dismutase 1. Conclusions Mitochondrial fusion is essential to cardiomyocyte mitochondrial function and regeneration. Reactive oxygen species are key mediators of cardiomyopathy in mitochondrial fusion-defective cardiomyocytes. Postulated mitochondrial-ER interactions mediated uniquely by mfn2 appear dispensable to functioning of the fly heart.

The reproductive tract of wild-caught male Boiga irregularis (Merrem, 1802) (Brown Treesnake) and the changes that result in these tissues from captivity are described. Wild-caught snakes were compared with snakes kept in captivity and sacrificed at approximately 10, 30, 50, and 60+ days. Snakes sacrificed after 10 days in captivity showed no differences in histological appearance or epithelial height in either the testis or sexual segment of the kidney (SSK) compared with wild snakes. Normal spermatogenic stages and SSK ultrastructure were observed in the testes and kidney from wild specimens and captive specimens after 10 days. In terms of the SSK, large electron-dense secretory vacuoles occupied the apices of the epithelial cells, while a basal nucleus, rough endoplasmic reticulum, and Golgi bodies filled the bases of these cells. All SSK cells were actively secretory in a mode that could most accurately be termed apocrine. At time of secretion, released vacuoles become diffuse and the apical membrane ruptures, spilling the SSK contents into the distal nephron lumen. Between 10 and 30 days in captivity, spermatogenesis and secretion in the SSK ceased and the epithelial height of both tissues decreased. At approximately 60 days, testicular epithelial height increased and spermatogenic activity was reestablished. The SSK, however, remained regressed at 60 days.