Search results
Results from the WOW.Com Content Network
The significance of mitochondrial fission and fusion is distinct for nonproliferating neurons, which are unable to survive without mitochondrial fission. Such nonproliferating neurons cause two human diseases known as dominant optic atrophy and Charcot Marie Tooth disease type 2A, which are both caused by fusion defects. Though the importance ...
Mitochondrial fission is the process by which mitochondria divide or segregate into two separate mitochondrial organelles. Mitochondrial fission is counteracted by mitochondrial fusion, where two mitochondria fuse together to form a larger one. [1] Fusion can result in elongated mitochondrial networks.
The processes of fission and fusion oppose each other and allow the mitochondrial network to constantly remodel itself. [9] [8] If a stimulus induces a change in the balance of fission and fusion in a cell, it could significantly alter the mitochondrial network.
In mammals MFN1 and MFN2 are essential for mitochondrial fusion. [7] In addition to the mitofusins, OPA1 regulates inner mitochondrial membrane fusion, and DRP1 is responsible for mitochondrial fission. [8] Mitofusin-2 (MFN2) is a mitochondrial membrane protein that plays a central role in regulating mitochondrial fusion and cell
Mitochondria routinely undergo fission and fusion events that maintain a dynamic reticular network. Drp1 is a fundamental component of mitochondrial fission. [12] Indeed, Drp1 deficient neurons have large, strongly interconnected mitochondria [13] due to dysfunctional fission machinery.
VPS35 and the retromer also help modulate mitochondrial fusion and fission. [ 9 ] [ 10 ] [ 16 ] In healthy conditions, VPS35 helps regulate mitochondrial fusion by removing mitochondrial E3 ubiquitin protein ligase 1 ( MUL1 ) from the outer mitochondrial membrane and preventing the degradation of mitofusin 2 ( Mfn2 ). [ 9 ]
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]
Evidence suggests that mitochondria can also undergo fusion and exchange (in a form of crossover) genetic material among each other. Mitochondria sometimes form large matrices in which fusion, fission, and protein exchanges are constantly occurring. mtDNA shared among mitochondria (despite the fact that they can undergo fusion). [citation needed]