Similar results were observed with the RUG3 mutant. Both mutants showed reduced root growth, small stature, and growth retardation. Another complex I mutant, ndufs4, also exhibited a similar phenotype. Although approximately one-third of mitochondrial ATP production is associated with complex I, the presence of alternative NADH dehydrogenases allows the electron transport chain to bypass complex I when complex I efficiency is reduced or when plants encounter stress. Interestingly, abo5, rug3 and ndufs4 plants produced viable seeds and propagated to the next generation, whereas mterf15 showed a more severe phenotype. Homozygous mterf15 plants showed a similar BMN673 PARP inhibitor phenotype as these mutants in terms of complex I deficiency; however, seeds from homozygous mterf15 plants could not germinate, even in solid medium over three months. It is possible that mTERF15 in maternal tissues of heterozygotic mterf15 embryo may partially contribute to the developing homozygous mterf15 seeds, which is completely absent in the developing seeds of homozygous mterf15 plants. This suggests that the germination defect of mterf15 is not only due to embryo lethality but also caused by aberrant reproductive organs, especially maternal tissues. The defective maternal tissues may reduce the flow of nutrient into the endosperm and eventually cause seed lethality. Therefore, mTERF15 may have additional roles in mitochondria, as observed in other eukaryotes, during embryogenesis and seed development. Here, we identify mTERF15 as an RNA-binding protein that is required for nad2 intron 3 splicing in mitochondria. The disruption of this splicing event leads to decreased complex I activity as well as growth and developmental retardation in mterf15 mutants. Further studies of the detailed mechanism of mTERF15 are required to reveal the molecular mechanisms involved in post-transcription regulation in Arabidopsis mitochondria. Osteoporosis is a common progressive bone disease that is characterized by decreased bone mineral density and is known to increase the risk of fractures. The disequilibration of bone resorption by osteoclasts and bone formation by osteoblasts underlies the pathogenesis of osteoporosis. At-risk populations for primary osteoporosis include elderly and postmenopausal women in particular because BMD is known to decrease with age and its rate of decline is very hormonally sensitive. Estrogen may exert anti-resorptive effects on bone in part by stimulating estrogen receptors and osteoprotegerin expression in osteoblasts. Estrogen is one of many proteins that are involved in the pathogenesis of osteoporosis. Age and external factors, such as smoking, body weight and race, also influence BMD, and more recently, investigators have found that genetic factors play important roles in the pathogenesis of osteoporosis. Twin and familial studies have indicated that 60–85% of BMD variance is genetically determined.