The dynamin-related GTPase Drp1 is required for embryonic and brain development in mice

By Junko Wakabayashi, Zhongyang Zhang, N. Wakabayashi, Y. Tamura, M. Fukaya, T. Kensler, M. Iijima, H. Sesaki. Journal of Cell Biology, 2009

682 citations recorded by the source corpus.

Brain-specific Drp1 knockout mice demonstrate that Drp1-mediated organelle division is important for development, mitochondrial morphogenesis, and apoptosis.

Subfields: Epidemiology, Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/81e7872ce7cb1de5f0af11a468c3b0ea031c3b0b

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Citations in the corpus

Mitochondria and cell death: outer membrane permeabilization and beyond (2010, background): “However, cells lacking DRP1 undergo MOMP, ruling out an absolute requirement for DRP1 for this even”
Impaired mitochondrial dynamics and abnormal interaction of amyloid beta with mitochondrial protein Drp1 in neurons from patients with Alzheimer's disease: implications for neuronal damage. (2011, background): “Further, recent studies of Drp1 knockout in mice revealed that double knockouts are embryonic lethal (37,38).”
Mitochondria and Mitophagy: The Yin and Yang of Cell Death Control (2012, background): “Deletion of Drp1 is embryonic-lethal, and myocytes in Drp1-null embryos have reduced contractility.(133) Defects in DRP1 function also are associated with early infant mortality and cardiomyopathy.”
Mitochondrial dynamics in health and disease: mechanisms and potential targets (2023, background): “38 53 Mitochondrial fusion Mitochondrial fusion includes several steps, starting with the activation of dynein-associated GTPases, including mitofusin (MFN) 1/2 on OMM, FAM73a/FAM73b and optic atrophy protein 1 (Opa1) on IMM, 54 – 56 followed by OMM fusion induced by GTP hydrolysis, subsequently…”
Mitochondria: In Sickness and in Health (2012, background): “…results in OXPHOS deficiencies, mtDNA loss, and mitochondrial motility defects, and division defects also cause OXPHOS deficiencies and significant increases in ROS production (Chen et al., 2003, 2007; Hermann et al., 1998; Ishihara et al., 2009; Parone et al., 2008; Wakabayashi et al., 2009).”
BAK/BAX macropores facilitate mitochondrial herniation and mtDNA efflux during apoptosis (2018, result): “In contrast, and as previously reported (51, 52), fission-deficient Drp1 cells at steady state exhibited a hyperfused mitochondrial network (fig.”