A hyperfused mitochondrial state achieved at G1–S regulates cyclin E buildup and entry into S phase

By K. Mitra, Christian Wunder, B. Roysam, Gang Lin, Jennifer Lippincott-Schwartz. Proceedings of the National Academy of Sciences of the United States of America, 2009

628 citations recorded by the source corpus.

Subfields: Cell Biology, Clinical Biochemistry, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/b98be7f35fcbb1203fc3faec1be09bcef1673880

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Citations in the corpus

Tubular network formation protects mitochondria from autophagosomal degradation during nutrient starvation (2011, methodology): “Mitochondrial fusion has been linked to increased ATP production during stress, starvation, and cell cycle (19, 22, 24).”
Fatty acid trafficking in starved cells: regulation by lipid droplet lipolysis, autophagy and mitochondrial fusion dynamics (2015, background): “Emerging evidence is also correlating the presence of fused mitochondria with many cellular states of high-energy demand, including G1/S cell-cycle transition (Mitra et al., 2009) and chemical stress (Tondera et al.”
Mitochondrial Dynamics in the Regulation of Nutrient Utilization and Energy Expenditure (2013, background): “Consequently, mitochondrial elongation during G1/S phase could permit high ATP synthesis rates that can sustain cell duplication (Mitra et al., 2009).”
Erk2 phosphorylation of Drp1 promotes mitochondrial fission and MAPK-driven tumor growth (2015, background): “There are a number of physiological mechanisms that could potentially explain the loss of tumor growth observed upon inhibition of Drp1, as the regulation of mitochondrial fusion and fission has been shown to play a role in several physiological processes whose dysregulation are classical ‘‘hallmark”
Metabolic regulation of mitochondrial dynamics (2016, background): “Elongated mitochondria have also been observed in other conditions associated with increased ATP production (Mitra et al., 2009; Tondera et al., 2009).”
A Unified Theory of Sepsis-Induced Acute Kidney Injury: Inflammation, microcirculatory dysfunction, bioenergetics and the tubular cell adaptation to injury (2014, neutral): “This mesh seems to be transient and specific to the G1-S transition, and mitochondria in this structure seem to act as syncytia, with electrical coupling and unusual hyperpolarization (66).”
Mitochondrial DNA mutations and human disease. (2010, background): “However, increasing reports on the relationship of mitochondrial function to the cell cycle [22–24] suggest a connection between mtDNA replication and the cell cycle may well actually exist.”