Extrachromosomal inheritance of oligomycin resistance in yeast.
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Journal Article↗
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Quantitative models of hybrid dysgenesis: rapid evolution under transposition, extrachromosomal inheritance, and fertility selection.
A model of the P-M system of hybrid dysgenesis is presented which incorporates single-site transposition of P factors in M cytotype, determination of offspring cytotype by both maternal cytotype and maternal or offspring nuclear genotype, and strong fertility selection in dysgenic individuals. The conditions required for the initial invasion of P factors into a pure M population, information concerning stable polymorphisms, and results of numerical iterations depicting the dynamic, nonequilibrium behavior of the system are summarized. While conditions for initial increase are independent of the rate of cytotype switching, the rate of evolution is accelerated by increased production of dysgenic individuals. If the transposition rate is sufficiently high to overcome the fertility barrier opposing P factors introduced into M populations, then convergence to high frequencies of the P factor occurs very rapidly. Under intense fertility depression, the phase of rapid increase may be preceded by an extended period of gradual increase at low frequencies.
Animals↗
Extrachromosomal inheritance controlling resistance to cadmium, cobalt, copper and zinc ions: evidence from curing in a Pseudomonas [proceedings].
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Cadmium↗
Inheritance of extrachromosomal ribosomal DNA during the asexual life cycle of Dictyostelium discoideum: examination by use of DNA polymorphisms.
Wild-type isolates of Dictyostelium discoideum exhibited differences in the size of restriction fragments of the extrachromosomal 88-kilobase ribosomal DNA (rDNA) palindrome. Polymorphisms in rDNA also were found among strains derived solely from the NC4 wild-type isolate. These variations involved EcoRI fragments II, III, and V; they included loss of the EcoRI site separating fragments II and V and deletion and insertion of DNA. More than one rDNA form can coexist in the same diploid or haploid cell. However, one or another parental rDNA tended to predominate in diploids constructed, using the parasexual cycle, between haploid NC4-derived strains and haploid wild-type isolates. In some cases, most if not all of the rDNA of such diploids were of one form after ca. 50 generations of growth. Segregant haploids, derived from diploids that possessed predominantly a single rDNA allele, possessed the same allele as the diploid and did not recover the other form. This evidence implies that replication does not proceed from a single chromosomal or extrachromosomal copy of the rDNA during the asexual life cycle of D. discoideum.
Alleles↗
Inheritance of the 2 micrometer m DNA plasmid from Saccharomyces.
A variety of Saccharomyces strains were examined for the presence of 2micro DNA and, if present, for the pattern of fragments produced by its digestion with site-specific (restriction) endonucleases. Two strains were found that did not contain detectable levels of 2micro DNA, and two strains contained 2micro DNA molecules having only one EcoRI restriction endonuclease recognition site rather than the usual two.-A haploid containing 2micro DNA with one EcoRI restriction site was mated with a haploid containing 2micro DNA with two EcoRI restriction sites and the resulting diploid maintained both types during vegetative growth. Sporulation of the diploid produced four spores, and the clones from these spores contained both types.-A haploid lacking 2micro DNA was mated with a haploid containing 2micro DNA and the resulting diploid contained 2micro DNA. The four clones derived from the haploid spores after sporulation of this diploid all contained 2micro DNA. A rho(-) strain without 2micro DNA was mated to a rho(+) strain with 2micro DNA, and heteroplasmons were selected that had received the nucleus from the strain without 2micro DNA and the mitochondria from the strain with 2micro DNA. Twelve of twenty-four such clones contained 2micro DNA.-I conclude that: (1) the different types of 2micro DNA identified in these strains do not restrict one another, (2) the different types are inherited extrachromosomally, (3) lack of 2micro DNA in two strains is not due to the absence of genes needed for maintenance and (4) the approximately 100 copies of 2micro DNA contained within a single cell are probably clustered within one or a few cytoplasmic organelles.
Cell Division↗
Chromosomal and extrachromosomal control of senescence in the ascomycete Podospora anserina.
In Podospora anserina senescence leading to cellular death occurs regularly after prolonged vegetative propagation. However, the life span of this ascomycete may be extended by various means: 1. Mutations in a least 8 morphogenetic genes belonging to 4 linkage groups postpone drastically or even prevent in certain pairwise combinations (e.g. i viv) the onset of senescence. 2. Inhibitors of mt DNA and of mitochondrial protein synthesis show a life prolonging effect when added in low concentrations to the growth medium. 3. A similar effect was found when mycelia were fed exclusively on non repressive carbon sources. Whereas the anti-aging effect of specific mutated genes is rather permanent, the life prolonging action of the inhibitors and carbon sources is restricted and temporary. These substances have no long lasting effect, since after their removal from the medium aging proceeds. Physiological experiments have further shown the existence of three phases in the life span of Podospora anserina. During the juvenile phase aging is prevented by all of these compounds; during the presenescent phase aging is prevented by inhibitors of mt DNA only, and during the senescent phase aging is irreversible. Senescence may be induced in juvenile protoplasts by DNA extracted from senescent mycelia. This, together with the well known fact that senescence is extrachromosomically inherited, points to extrachromosomal DNA as the causative agent of senescence. This kind of DNA may be connected with or perhaps located in the mitochondria. Collectively, the data are consistent in showing that the syndrome of senescence in Podospora anserina is controlled by a chromosomal-extrachromosomal interaction. In this system, extrachromosomal DNA, perhaps a mt DNA, is identical with the infectious principle initiating the decay of the cell, and nuclear genes supervise its expression.
Aging↗
Maternal inheritance of extrachromosomal DNA in malaria parasites.
Plasmodium falciparum has two extrachromosomal genomes, the mitochondrial 6-kb DNA element and the 35-kb circular DNA. The mitochondrial gene cytochrome b on the 6-kb element has been shown to be inherited uniparentally. In order to ascertain whether the route is maternal or paternal we have examined preparations of male and female gametes of the closely related Plasmodium gallinaceum for the presence of extrachromosomal DNA. DNA from purified preparations of gametes was hybridised to probes for both the 6-kb and 35-kb extrachromosomal genomes. Both probes hybridised to the preparation of Plasmodium gallinaceum female gametes but not to that of the males. We conclude that the extrachromosomal DNAs of malaria parasites are transmitted maternally.
Animals↗
Inheritance of extrachromosomal rDNA in Physarum polycephalum.
In the acellular slime mold Physarum polycephalum, the several hundred genes coding for rRNA are located on linear extrachromosomal DNA molecules of a discrete size, 60 kilobases. Each molecule contains two genes that are arranged in a palindromic fashion and separated by a central spacer region. We investigated how rDNA is inherited after meiosis. Two Physarum amoebal strains, each with an rDNA recognizable by its restriction endonuclease cleavage pattern, were mated, the resulting diploid plasmodium was induced to sporulate, and haploid progeny clones were isolated from the germinated spores. The type of rDNA in each was analyzed by blotting hybridization, with cloned rDNA sequences used as probes. This analysis showed that rDNA was inherited in an all-or-nothing fashion; that is, progeny clones contained one or the other parental rDNA type, but not both. However, the rDNA did not segregate in a simple Mendelian way; one rDNA type was inherited more frequently than the other. The same rDNA type was also in excess in the diploid plasmodium before meiosis, and the relative proportions of the two rDNAs changed after continued plasmodial growth. The proportion of the two rDNA types in the population of progeny clones reflected the proportion in the parent plasmodium before meoisis. The rDNAs in many of the progeny clones contained specific deletions of some of the inverted repeat sequences at the central palindromic symmetry axis. To explain the pattern of inheritance of Physarum rDNA, we postulate that a single copy of rDNA is inserted into each spore or is selectively replicated after meiosis.
Extrachromosomal Inheritance↗
An extrachromosomal factor causing loss of paternal chromosomes.
Extrachromosomal inheritance is ubiquitous among plants and animals; however, most extrachromosomal factors are uniparentally inherited through females, but not through males. Examples include chloroplasts, mitochondria and a variety of intracellular symbionts. The only known exception to maternal extrachromosomal inheritance in an animal is a paternally transmitted sex ratio factor (psr) which causes all-male families in the parasitic wasp, Nasonia vitripennis. Normally in this wasp, male offspring are haploid and develop from unfertilized eggs whereas females are diploid and develop from fertilized eggs. The psr factor is either a venereally transmitted infection which prevents egg fertilization (and therefore causes all-male families), or a factor transmitted to eggs by the sperm of males carrying psr, which somehow prevents incorporation of the paternal chromosomes. Here we report that sperm from psr males fertilizes eggs, but that the paternal chromosomes are subsequently condensed into a chromatin mass before the first mitotic division of the egg and do not participate in further divisions. Resulting haploid offspring are male, but have inherited the paternal factor. This extrachromosomal factor promotes its own transmission at the expense of the paternal chromosomes, and therefore can be considered a 'selfish' genetic element.
Animals↗
The extrachromosomal control of nonsense suppression in yeast: an analysis of the elimination of [psi+] in the presence of a nuclear gene PNM.
When a [psi-] strain of yeast mutates to [psi+], the efficiency of suppression by certain ochre suppressors is increased. The [psi+] phenotype is inherited extrachromosomally. There is a nuclear gene, PNM, which, when mutant, causes loss of the [psi+] phenotype. PNM- is dominant to PNM+ and a heterozygous diploid gradually loses the ability over successive generations, to produce PNM+ [psi+] spores. This paper describes the kinetics of this elimination and the data obtained are discussed in relation to two models of the molecular nature of the [psi] genetic determinant--one considering the [psi] determinant as an autonomous nucleic acid, the other treating the possibility that the [psi] nucleic acid is that which codes for rRNA in the nuclear genome.
Cell Division↗
A genetic study of a Staphylococus aureus plasmid involving cure and transference.
High frequency transfer and elimination of drug resistance may indicate an extrachromosomal inheritance of genetic determinants. This study shows the cure and transfer of a small plasmid and tetracycline resistance in Staphylococcus aureus 1030 (55)Tet strains. Several methods are available for plasmid elimination. We used ethidium bromide, an agent that binds to DNA, and thus inhibits DNA polymerase. This caused a high frequency of loss of the small plasmid and resistance to tetracycline. Transfer of tetracycline resistance was done in a mixed culture at a frequency of 10(-6). This type of study is very important to physicians and epidemiology investigators and provides better knowledge on antibiotic-resistance mechanisms that may occur in vivo in a hospital environment.
Conjugation, Genetic↗
Clinical aspects of gene expression.
1. Expression and nonexpressin of genetic information may be viewed in relationship to the biologic structures that express or do not express the genetic information. We suggest defining expressivity as the quality of expression of genetic information in cells, tissues, organs, etc, of individuals, defining penetrance as the quality of expression of genetic information in an individual organism as a whole, and using a new term, phenotrance, to describe the quality of expression of genetic information in generations. 2. Decreased phenotrance may be indicated by "incompletely dominant" inheritance, by conditions for which "dominant" as well as "recessive" inheritance has been reported, or by disorders with sporadic occurrence in most and familial occurrence in some instances. The human conditions with decreased phenotrance that we have studied indicate that there are different types of decreased phenotrance. 3. The mechanisms for decreased phenotrance in man may correspond to certain genetic mechanisms that have been studied in lower organisms, such as delayed mutation, replicating instabilities, controlling elements, extrachromosomal inheritance, and others.
Achondroplasia↗
Manifestation of carcinogenesis as a stochastic process on the basis of an altered mitochondrial genome.
Computer calculations are used to show the feasibility of a concept which explains the manifestation of a pathological cell function from a latent state by the phenomenon of extrachromosomal inheritance (through the mitochondrial genome) in mammalian cells. A hypothesis is submitted in which this principle is applied to the process of carcinogenesis. According to this concept, the manifestation of a tumor cell--after the initiation stage--entirely depends on stochastic events, i.e., random distribution of mitochondria during cell divisions, with an accumulation of the lesion in a few out of many cells. We feel that this concept comprises a better explanation of many characteristics and peculiarities of the phenomenon of carcinogenesis than do attempts which explain tumor formation as a phenomenon caused by mutation in a nuclear genome. A consideration of the principles presented automatically leads to a number of specific consequences with regard to carcinogenesis. Some of these consequences are discussed. They include: 1. the process of malignant transformation should not be irreversible for all the cells of a progeny; 2. the number of mitochondria in a cell type should be inversely correlated to tumor frequency; 3. the latent period should mainly be determined by the cell division rate and the "extent" of the initiating event; 4. susceptibility to carcinogenesis may be substantially higher if the number of mitochondria per cell line is increasing or decreasing, i.e., during the embryonic and fetal periods; 5. heterogeneous types of cells may arise from a single "initiated" cell, and 6. the process of malignant transformation should not necessarily be confined to one generation of the species. In addition, experimental approaches to support the submitted concept are suggested.
Animals↗
Two changes of the same nucleotide confer resistance to diuron and antimycin in the mitochondrial cytochrome b gene of Schizosaccharomyces pombe.
Diuron (3-(3,4-dichlorophenyl)-1,1-dimethylurea) and antimycin, both inhibitors of mitochondrial respiration, block electron flow between cytochromes b and c1. Mutants resistant to either drug have been selected using Schizosaccharomyces pombe strains with an extrachromosomally inherited mutator. In analogy to Saccharomyces cerevisiae these mutational sites were assumed to map in the cytochrome b gene. DNA sequence analysis showed that two changes in the same nucleotide are responsible for resistance to antimycin and diuron. Analysis of resistant and sensitive progeny of crosses between the mutants and the wild type confirmed the correlation between mutational alteration and resistant phenotype.
Amino Acid Sequence↗
Genomic imprinting: a possible mechanism for the parental origin effect in Huntington's chorea.
Huntington's disease (HD) is an autosomal dominant condition with almost complete penetrance. The age of onset of the symptoms, however, is variable and depends on the parental origin of the gene. A high proportion of early onset cases inherit the HD gene from their father, whereas a considerable proportion of late onset cases inherit the gene from their mother. Modification of the HD gene by maternally inherited extrachromosomal factors has been invoked to account for the parental origin effect. Recent experimental evidence suggests genomic imprinting as an alternative mechanism, by which the gene itself becomes modified in a different way depending on whether it is passed through the maternal or the paternal germline. This modification may involve methylation of DNA and could result in earlier or higher level expression of the gene when it is transmitted by the father.
Age Factors↗
Tyrosinase activity in Streptomyces glaucescens is controlled by three chromosomal loci.
In Streptomyces glaucescens the production of the enzyme tyrosinase (EC 1.14.18.1) is controlled by at least three loci: MELA, MELB, and MELC. Mutations in MELA and MELB are rare. They both map on the S. glaucescens chromosome in the interval between the markers leu-2 and ura-3. MELC, however, shows an exceptionally high mutation rate. MelC strains arise spontaneously with a frequency of about 0.1%, and they can be specifically induced with ethidium bromide, acridine orange, or by prolonged storage of spores or mycelium at 4 degrees C. Ultraviolet (UV) irradiation or treatment with N-methyl-N'-nitro-N-nitrosoguanidine under conditions which induce auxotrophic mutations, however, do not specifically induce the appearance of tyrosinase-negative strains. Most, but not all, of the melC strains acquire additional mutations which make them sensitive to streptomycin (strS) and unable to produce hydroxystreptomycin. Mapping of the mutations classified as melC proves to be difficult. Some of the matings indicate a map position between his-2 and pro-1, while others, all highly unbalanced crosses, can not be analyzed in a meaningful way because of abnormal segregation of the reference markers. This is probably due to some of the additional mutations which occur frequently with the melC mutations and not to extrachromosomal inheritance of MELC.
Alleles↗
Plasmids in Listeria monocytogenes and other Listeria species.
One hundred and twenty-two food, clinical, and veterinary strains of Listeria monocytogenes were examined for the presence of plasmids. Twenty-five (20%) contained plasmids, which varied from 1.3 to 66 MDa in size. Of 10 strains of other Listeria species (L. innocua, L. ivanovii, L. welshimeri, L. seeligeri, L. grayi, and L. murrayi) examined, seven (70%) contained plasmids, varying from 38 to 53 MDa. No strains with multiple plasmids were found. Plasmids of identical size were isolated from related strains in some, although not all, cases. The presence of a plasmid in a strain was not related to phenotypic characters of known extrachromosomal inheritance.
Animals↗
[Method for studying horizontal transfer of plasmids in Erwinia carotovora].
A simple method to determine frequency characteristics of the horizontal transfer of antibiotic resistance by transconjugative plasmids of various incompatibility groups into Erwinia carotovora strains has been developed. The proposed method for selection of E. carotovora transconjugates provides for the use of selective medium with pectin and corresponding antibiotic, which permits carrying out reliable counterselection of the donor (Escherichia, Salmonella). The proposed method helped to study horizontal transfer of plasmids RP4 (Inc P), R 391 (Inc J) and pKM101 (Inc N) to some E. carotovora strains and to demonstrate their inheritance as extrachromosomal DNA in Erwinia cells.
Anti-Bacterial Agents↗