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A crista (/ ˈ k r ɪ s t ə /; pl.: cristae) is a fold in the inner membrane of a mitochondrion. The name is from the Latin for crest or plume , and it gives the inner membrane its characteristic wrinkled shape, providing a large amount of surface area for chemical reactions to occur on.
This ratio is variable and mitochondria from cells that have a greater demand for ATP, such as muscle cells, contain even more cristae. Cristae membranes are studded on the matrix side with small round protein complexes known as F 1 particles, the site of proton-gradient driven ATP synthesis. Cristae affect overall chemiosmotic function of ...
Dynamin-like 120 kDa protein, mitochondrial is a protein that in humans is encoded by the OPA1 gene. [5] [6] This protein regulates mitochondrial fusion and cristae structure in the inner mitochondrial membrane (IMM) and contributes to ATP synthesis and apoptosis, [7] [8] [9] and small, round mitochondria. [10]
[4] [5] It is enriched at cristae junctions in the intermembrane space of the mitochondria. [1] The structure of the protein contains a nonstructured N-terminal region, a hydrophobic helix and a C-terminal CHCH domain which contains a Cx(9)C motif and two additional cysteines. A total of four cysteines are predicted to form two disulfide bonds. [6]
OPA1 plays both a genetic and molecular role in mitochondrial fusion and in cristae remodeling during apoptosis. [5] OPA1 exists in two forms; the first being soluble and found in the intermembrane space, and the second as an integral inner membrane form, work together to restructure and shape the cristae during and after apoptosis.
IMMT encodes an inner mitochondrial membrane (IMM) protein in the nucleus. It is posttranslational transported to the IMM. Mic60/Mitofilin (encoded by the IMMT gene) is a core subunit of the MICOS-complex, directly located next to cristae junctions (CJ). Human Mic60 exists in two isoforms of different size, anchored to the IMM via its N ...
This part of the enzyme is located in the mitochondrial inner membrane and couples proton translocation to the rotation that causes ATP synthesis in the F 1 region. In eukaryotes, mitochondrial F O forms membrane-bending dimers. These dimers self-arrange into long rows at the end of the cristae, possibly the first step of cristae formation. [12]
His lab identified the role of Opa1, optic atrophy protein 1, in holding mitochondrial cristae junctions tight, [6] [7] which is an important determinant of mitochondrial respiratory efficiency. [8] His lab also found augmentation of Opa1 to correct mitochondrial diseases and blunt muscular atrophy, [ 9 ] stroke and heart ischemia. [ 10 ]