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The below mentioned article provides a study note on Inheritance of Mitochondria.
Introduction to the Inheritance of Mitochondria:
Mitochondria are the cytoplasmic organelles which contain various respiratory enzymes and are main source of energy for the cell. They are found in cell in variable numbers. The complexity of structure of the mitochondria and their similarity in some ways to plastids suggest the possibility that they may be inherited in the same way as the plastids.
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The mitochondria have a double membrane and contain besides respiratory enzymes of electron transport chain (the cytochromes), their own genetic determinants (DNA). There is certain amount of electron micrographic evidence for the continuity of this cytoplasmic organelle through cell division.
Although most of the mitochondrial proteins and enzymes are produced by nuclear genes, yet nearly 20% of them result due to activity of mitochondrial genes.
The fact that mitochondrion contains its own DNA has led some to speculate that it evolved from symbiotic micro-organism that gradually lost the ability to exist independently. There is enough evidence in support of this. But, some people disagree with this. Mitochondria cannot be regarded truly autonomous cytoplasmic organelles as they require both their own genes and nuclear genes in order to exist.
The mitochondrial heredity has been exemplified by yeast (saccharomyces cereviceae) and neurospora crassa.
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Ephrussi’s Experiment with Yeast:
Certain strains of yeast (s. cereviceae) produce tiny colonies when grown on agar medium. Ephrussi (1953) observed that one or two out of every one thousand colonies were only about one-third or one- half of the diameter of the remainder. The small colonies are termed as petite colonies.
Cells from the normal large colonies, when spread on culture medium, further produced a small proportion of petite colonies and this happened so time after time. The cells from the small colonies were true breeding and they produced only petites.
Biochemical studies have established that the slow growth of petite colonies was due to the loss of aerobic respiratory enzymes particularly cytochrome a and b and enzyme cytochrome oxidase occurring in mitochondria of the cells and the utilization of the less efficient fermentation process by the cells.
The petite phenotype can result either from mutation of nuclear genes or from mitochondrial genes. Petite mutants resulted due to mutation in a nuclear gene follow Mendelian pattern of inheritance with segregation occurring in heterozygotes.
This type of petite mutation is called segregational petite or nuclear petite. When the individuals of petite colony are crossed to the individuals from normal large sized colony, normal zygotes are formed which produce normal cells vegetatively.
When meiosis takes place in diploid cells, haploid cells are recovered that will form petite and normal colonies in 1: 1 ratio as shown below:
Such any colonies are formed evidently due to mutant nuclear genes, they are called segregational petites.
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Bores Ephrussi and his associates (1953) also found that in presence of small amount of acridine dyes such as acriflavine and euflavine many cytochrome deficient petite colonies developed which showed extra-chromosomal (Non Mendelian) inheritance for petite characters. They were called vegetative petites.
The rate of mutation was much higher at low concentrations than that normally expected for chromosomal mutation. The vegetative petites may arise directly from mutations in mitochondrial genes leading to defective mitochondria.
There are two classes of vegetative or extra-chromosomal petites:
(i) Neutral petites; and
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(ii) Suppressive petites, which show different patterns of inheritance.
Neutral Extra-chromosomal or Vegetative Petites:
When a cross is made between wild type haploid yeast and neutral petite haploid yeast, normal diploid offsprings are obtained. The diploid individuals by budding process produce several normal diploids. When meiosis occurs in normal diploids, haploid ascospores are formed which produce normal haploid colonies.
If the determinants of this trait were chromosomal, one would expect normal and petite traits in 1:1 ratio in the population of haploid spore cells. This suggests that the inheritance is non-chromosomal.
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The genetic basis of this type of inheritance can be explained assuming the presence of an extra-chromosomal or cytoplasmic factor [rho+] in normal strain and missing or [rho–[N]] in neutral petite mutants. The neutral petites [rho–[N]] usually lack in mitochondrial DNA. Now, if the haploid neutral petite is crossed to haploid normal strain, the diploid would be normal.
The normal condition in diploid cells appears because of normal mitochondria with [rho+] factor contributed by normal haploid strain. These normal mitochondria replicate and are passed on to haploid spores after meiosis in diploid cells. The mitochondria contributed by neutral petite mutant possibly do not replicate and gradually degenerate. So all the haploid spores and their descendants would be normal.
The pattern of inheritance is as follows:
Inheritance Pattern of Suppressive Petites:
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The suppressive petite mutant shows different behaviour than the neutral petite. When a cross is made between haploid cells of suppressive petite and haploid cells of normal strain, diploid cells are obtained which are in part normal and in part petite and as their name indicates, they can suppress normal aerobic respiration in presence of normal cytoplasm.
The normal diploids after meiosis produce normal haploid spores while the diploid petites after budding produce diploids which may be all petites or some normal and some petites. Normal diploids after sporulation produce only normal and no petite.
It is thus obvious that suppressive petites follow Non-Mendelian pattern of inheritance. The genetic basis of this type of inheritance can be explained by assuming the presence of an extra-chromosomal factor [rho+] in normal strain and [rho–[s]] in suppressive petites.
The genetic cause for suppressive petite is mitochondrial mutation. Unlike neutral petites, the mitochondria of suppressive petites contain mutant DNA. The mutant mitochondria can replicate and can be passed on to the progeny cells which can, in turn, express mutant phenotype. In the cross in question it is the relative proportion of normal and mutant mitochondria that determines the phenotype of the particular cell.
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The diploid cells and haploid spores would be normal if normal mitochondria predominated and they would show mutant phenotype if mutant mitochondria predominated. The lack of normal segregation and also the high mutability of normal colony cells provide good evidence that vegetative petite phenotype is due to extra-chromosomal or cytoplasmic genes.
The Poky Strain in Neurospora:
There are several examples for mitochondrial enzyme deficiency which are cases of extra-chromosomal inheritance. One of the classical examples of extra-chromosomal inheritance of plasma genes came from studies of neurospora.
In this fungus, there is a slow growing mutant strain called poky. The mitochondria contain cytochromes a, b and c which are electron transport proteins necessary for oxidative phosporylation.
In poky strains, either cytochrome a or cytochrome b is absent but cytochrome c is present in excess. Poky differs from petite in that the two mutants are not deficient for the same enzymes. When poky as female parent was crossed with a normal strain as a male parent, the progeny were found to be poky.
In reciprocal cross (normal poky ♀× poky ♂), the progeny were normal. This Non-Mendelian uniparental inheritance suggested that the cytoplasm of female parent was important because the only difference between reciprocal crosses was in contribution of cytoplasm.
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The male gametes in neurospora contribute negligible amount of cytoplasm just as in animals or higher plants. So, it is probable that the factor for pokyness resided somewhere in the cytoplasm. The segregation of poky from normal is never observed and the progeny of poky ♀× normal ♂ of will always be poky. Thus nuclear genotype has no effect on this particular phenotype.
