Mitochondrial fission factor

MFF
Identifiers
Aliases	MFF, C2orf33, GL004, mitochondrial fission factor, EMPF2
External IDs	OMIM: 614785; MGI: 1922984; HomoloGene: 137341; GeneCards: MFF; OMA:MFF - orthologs
Gene location (Human) Chr. Chromosome 2 (human)[1] Band 2q36.3 Start 227,325,151 bp[1] End 227,357,836 bp[1]
Gene location (Mouse) Chr. Chromosome 1 (mouse)[2] Band 1|1 C5 Start 82,702,611 bp[2] End 82,730,115 bp[2]
RNA expression pattern Bgee Human Mouse (ortholog) Top expressed in sperm left testis right testis gonad ganglionic eminence C1 segment body of pancreas Brodmann area 9 anterior cingulate cortex prefrontal cortex Top expressed in Epithelium of choroid plexus barrel cortex medullary collecting duct iris substantia nigra medial ganglionic eminence ventral tegmental area retinal pigment epithelium medial vestibular nucleus renal corpuscle More reference expression data BioGPS n/a
Gene ontology Molecular function protein homodimerization activity protein binding Cellular component integral component of membrane membrane synaptic vesicle peroxisome synapse mitochondrial outer membrane cell junction integral component of mitochondrial membrane cytoplasmic vesicle mitochondrion Biological process mitochondrial fusion mitochondrial fragmentation involved in apoptotic process positive regulation of mitochondrial fission mitochondrial fission regulation of mitochondrion organization regulation of peroxisome organization protein targeting to mitochondrion peroxisome fission positive regulation of release of cytochrome c from mitochondria mitochondrion morphogenesis protein homooligomerization release of cytochrome c from mitochondria positive regulation of protein targeting to membrane Sources:Amigo / QuickGO
Orthologs Species Human Mouse Entrez 56947 75734 Ensembl ENSG00000168958 ENSMUSG00000026150 UniProt Q9GZY8 Q6PCP5 RefSeq (mRNA) NM_001277061 NM_001277062 NM_001277063 NM_001277064 NM_001277065 NM_001277066 NM_001277067 NM_001277068 NM_020194 NM_029409 NM_001310695 NM_001310697 NM_001310699 NM_001372405 NM_001372406 NM_001372407 NM_001372408 NM_001372409 NM_001372411 NM_001372412 NM_001372413 NM_001372414 RefSeq (protein) NP_001263990 NP_001263991 NP_001263992 NP_001263993 NP_001263994 NP_001263995 NP_001263996 NP_001263997 NP_064579 NP_001297624 NP_001297626 NP_001297628 NP_083685 NP_001359334 NP_001359335 NP_001359336 NP_001359337 NP_001359338 NP_001359340 NP_001359341 NP_001359342 NP_001359343 Location (UCSC) Chr 2: 227.33 – 227.36 Mb Chr 1: 82.7 – 82.73 Mb PubMed search [3] [4]
Wikidata
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Mitochondrial fission factor (Mff) is a protein that in humans is encoded by the MFF gene.^[5] Its primary role is in controlling the division of mitochondria. Mitochondrial morphology changes by continuous fission in order to create interconnected network of mitochondria. This activity is crucial for normal function of mitochondria.^[6] Mff is anchored to the mitochondrial outer membrane through the C-terminal transmembrane domain, extruding the bulk of the N-terminal portion containing two short amino acid repeats in the N-terminal half and a coiled-coil domain just upstream of the transmembrane domain into the cytosol.^[7] It has also been shown to regulate peroxisome morphology.^[8]

Mff is an outer mitochondrial membrane protein that binds to the GTPase Drp1; the Mff-Drp1 complex is what promotes mitochondrial fission. Knockdown of Mff causes the mitochondrial network to expand (by releasing the Drp1 foci from the outer mitochondrial membrane), while Mff overexpression causes it to become fragmented (by stimulating mitochondrial recruitment of Drp1).^[9] DRP1 is mainly cytosolic, but translocate to the mitochondrial surface in order to mediate fission of mitochondria.^[6] Mitochondrial fission factor plays a crucial role in engaging Drp1 to the outer mitochondrial membrane in order to direct mitochondrial fission.^[6] Mff overexpression leads to various defective conditions in humans such as neurogenerative disorders like Huntington’s disease, Alzheimer’s disease, metabolic disorders, cardiovascular disease and majorly cancer. re-fusing mitochondria may be a viable therapeutic strategy in diseases with excessive mitochondrial fission.^[10]