mitochondria is found in eukaryotic cells.
mitochondria is found in eukaryotic cells.
mitochondria is found in what type of cells?
eukaryotic
the hypothesis differs from many alternative views within the endosymbiotic theory framework, which suggest that the first eukaryotic cells evolved a nucleus but lacked mitochondria, the latter arising as a eukaryote engulfed a primitive bacterium that eventually became the mitochondrion. the hypothesis attaches evolutionary significance to hydrogenosomes and provides a rationale for their common ancestry with mitochondria. hydrogenosomes are anaerobic mitochondria that produce atp by, as a rule, converting pyruvate into hydrogen, carbon dioxide and acetate. examples from modern biology are known where methanogens cluster around hydrogenosomes within eukaryotic cells. most theories within the endosymbiotic theory framework do not address the common ancestry of mitochondria and hydrogenosomes. the hypothesis provides a straightforward explanation for the observation that eukaryotes are genetic chimeras with genes of archaeal and eubacterial ancestry. furthermore, it would imply that archaea and eukarya split after the modern groups of archaea appeared. most theories within the endosymbiotic theory framework predict that some eukaryotes never possessed mitochondria. the hydrogen hypothesis predicts that no primitively mitochondrion-lacking eukaryotes ever existed. in the 15 years following the publication of the hydrogen hypothesis, this specific prediction has been tested many times and found to be in agreement with observation.
hydrogen hypothesis
transfer of the released mtdna into the nucleus: the first step in the transferring process is the release of mtdna into the cytoplasm. thorsness and fox demonstrated the rate of relocation of mtdna from mitochondria into the nucleus using "ura3- " yeast strain with an engineered "ura3 "plasmid, required gene for uracil biosynthesis, in the mitochondria. during the propagation of such yeast strains carrying a nuclear "ura3 " mutation, plasmid dna that escapes from the mitochondrion to the nucleus, complements the uracil biosynthetic defect, restoring growth in the absence of uracil, and easily scored phenotype. the rate of dna transfer from the mitochondria to the nucleus was estimated as 2 x 10-5 per cell per generation while the opposite, in the case of "cox2" mutant, the rate of the transfer of plasmid from the nucleus to the mitochondria is apparently at least 100,000 times less. many factors control the rate of mtdna escapes from mitochondria to the nucleus. the higher rate of mutation in mtdna in comparison with ndna in the cells of many organisms is an important factor promoting the transfer of mitochondrial genes into the nuclear genome. one of the intergenic factors results in the higher destruction rate of mitochondrial macromolecules, including mtdna, is the presence of high level of reactive oxygen species (ros), generated in mitochondria as the by-products in atp synthesis mechanism. some other factors influencing the escape of mtdna from mitochondria include the action of mutagenic agents and other forms of cellular stress that can damage mitochondria or their membranes, which proves that is possible to assume that exogenous damaging agents (ionizing radiation and chemical genotoxic agents) increase the rate of mtdna escape into the cytoplasm. thorsness and fox continued their research to find the endogenous factors affecting mtdna escape into the nucleus. they isolated and studied 21 nuclear mutants with different combinations of mutations in at least 12 nuclear loci called the "yme" (yeast mitochondrial escape) mutations, in different environmental conditions since some of these mutations cause temperature sensitivity. they found out these mutations which perturb mitochondrial functions, due to the alteration of gene products, affect mitochondrial integrity and led to mtdna escape to the cytoplasm. additionally, defects in the proteins change the rate of mtdna transfer into the nucleus. for instance, in the case of "yme1 "mutant, abnormal mitochondria are targeted for degradation by the vacuole, with the help of "pep4 ", a major proteinase, and degradation increases mtdna escape to the nucleus through the process of mitophagy. in addition, thorsness and campbell found that by disruption of "pep4", the frequency of mtdna escape in "yme1" strains decreases. similarly, the disruption of "prc1", which encodes carboxypeptidase y, lowers the rate of mtdna escape in "yme1" yeast. evidence shows that mitophagy is one of the possible ways for mtdna transfer into the nucleus and determined to be the most supported pathway up to now. some other possible pathways are shown in figure 1. the first pathway, as it was explained, is a "yme1"mutant that results in inactivation of "yme1p" protein, a mitochondrial-localized atp-dependent metalloproteinase, leading to high escape rate of mtdna to the nucleus. mitochondria of "yme1" strain are taken up for degradation by the vacuole more frequently than the wild-type strain. moreover, cytological investigations have suggested several other possible pathways in the diverse number of species, including a lysis of the mitochondrial compartment, direct physical connection and membrane fusion between mitochondria and nucleus, and encapsulation of mitochondrial compartments inside the nucleus, as shown in figure 1.
numt