[Genetic crossing of strains of Escherichia coli indicated by production of colicine I].
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Anti-Bacterial Agents↗
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Results for “Crossing Over, Genetic”
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A genetic linkage map of the mouse using restriction landmark genomic scanning (RLGS).
We have developed a multiplex method of genome analysis, restriction landmark genomic scanning (RLGS) that has been used to construct genetic maps in mice. Restriction landmarks are end-labeled restriction fragments of genomic DNA that are separated by using high resolution, two-dimensional gel electrophoresis identifying as many as two thousand landmark loci in a single gel. Variation for several hundred of these loci has been identified between laboratory strains and between these strains and Mus spretus. The segregation of more than 1100 RLGS loci has been analyzed in recombinant inbred (RI) strains and in two separate interspecific genetic crosses. Genetic maps have been derived that link 1045 RLGS loci to reference loci on all of the autosomes and the X chromosome of the mouse genome. The RLGS method can be applied to genome analysis in many different organisms to identify genomic loci because it uses end-labeling of restriction landmarks rather than probe hybridization. Different combinations of restriction enzymes yield different sets of RLGS loci providing expanded power for genetic mapping.
Animals↗
Tagging of genes involved in multidrug resistance in Aspergillus nidulans.
We have used a plasmid containing the Neurospora crassa pyr4 gene to transform an Aspergillus nidulans pyrG89 mutant strain in the presence of Bam-HI, and isolated multidrug-sensitive mutants among the transformants. Using this approach, we hoped to identify genes whose products are important for drug resistance by analyzing gene disruptions that alter the drug sensitivity of the cell. About 1300 transformants isolated following transformation were screened for sensitivity to drugs or various stress agents with different and/or the same mechanism of action. Seventy-seven of these transformants showed sensitivity to at least one drug, while fourteen transformants showed a complex phenotype of sensitivity to different drugs. The pyr4 marker was shown to be tightly linked to the mutant phenotype in only 36% of the pleiotropic mutants analyzed in sexual crosses. Genetic crosses between our multidrug-sensitive transformants and cycloheximide-sensitive and imazalil-resistant mutants of A nidulans were performed to determine whether mutations were present at the same loci. We have shown that the gene imaD that confers resistance to imazalil may also be involved in cycloheximide and hygromycin sensitivity, since this mutation is allelic to scyB (mutant scy290). In addition, the cross between the transformant R223 and the imazalil-resistant mutant ima535 showed that both mutations are in the same complementation group, suggesting that the gene imaG could also be involved in cycloheximide and itraconazole sensitivity.
Anti-Bacterial Agents↗
Linkage Group Selection--a fast approach to the genetic analysis of malaria parasites.
Genetic analysis of malaria parasites has shown that the mechanisms of inheritance in these organisms are classically Mendelian. In other words, alleles of genes at different loci recombine, and alleles at the same gene locus segregate, in the progeny of a genetic cross between two genetically distinct lines of malaria parasite. Importantly, such progeny are haploid in the first filial generation following genetic crossing. Consequently, genetic analysis, including linkage analysis, can be done directly upon the cloned cross progeny. Linkage analysis conducted upon the progeny of genetic crosses between malaria parasites can lead to the location of a single gene controlling a specific phenotype, as has been achieved to identify the gene for chloroquine resistance in Plasmodium falciparum. The work involved, however, is extremely labour intensive. It involves the generation of many hundreds, to a thousand or so, of independent recombinant clones from the cross progeny and the biological characterisation, and genetic typing for hundreds of molecular genetic markers of each such clone. We discuss here a fast-track method for identifying genes controlling specific phenotypes, e.g. drug resistance/sensitivity. It involves the mass screening with quantitative molecular genetic markers of the uncloned progeny of a genetic cross following its growth under a selection pressure representing the phenotype of interest. We have called the method Linkage Group Selection.
Animals↗
Genetic determination of cardiac mass in normotensive rats: results from an F344xWKY cross.
Genetic determinants affect adult cardiac mass and the predisposition to develop cardiac hypertrophy. The aim of this study was to identify quantitative trait loci (QTL) that control heart and left ventricular (LV) weight by use of normotensive inbred rat strains that differ in their adult cardiac mass phenotype. We studied 126 male F2 rats derived from a cross of normotensive Wistar-Kyoto and Fischer 344 rats. At 12 weeks of age, total heart weight and LV weight were measured. Genomic DNA from these animals was screened by use of polymorphic microsatellite markers across the whole genome (excluding the sex chromosomes). In this cross, the genetic contribution to total heart weight variation was 56%, and the genetic contribution for LV weight was 55%. Using the Mapmaker/QTL computer package, we identified a significant QTL on chromosome 3 with a log10 likelihood (LOD) score of 4.8, which accounted for 16.5% of the total variance of LV weight. This QTL was centered close to the marker D3Rat29. The QTL was also found to be significantly linked with total heart weight (LOD=4.4). These data provide the first demonstration of a QTL on chromosome 3 that plays a role in determining the difference in LV mass between normotensive Fischer 344 and Wistar- Kyoto inbred rat strains. The prostaglandin synthase 1 gene is located within the QTL.
Animals↗
The unexpected recovery of hybrids in a Drosophila species cross: a genetic analysis.
The species cross between Drosophila melanogaster and D. simulans was first described by Sturtevant in the 1920s. According to his description, the hybridization of D. simulans females and D. melanogaster males produces only (or almost only) male progeny. Female hybrids are embryonic lethal. Here it is shown that these traditional results no longer hold. Instead, D. simulans is polymorphic for factor(s) that qualitatively affect the outcome of species crosses to D. melanogaster. Remarkably, many, if not most, strains of D. simulans produce abundant female hybrids when crossed to D. melanogaster males. Genetic analysis of the difference between D. simulans strains that produce many versus few hybrid females shows that recovery of hybrid females depends on autosomal, maternally acting gene(s).
Animals↗
Distinct QTLs are linked to cardiac left ventricular mass in a sex-specific manner in a normotensive inbred rat inter-cross.
Genetic mapping of the progeny of an F(2) inter-cross between WKY and WKHA rats had previously allowed us to detect male-specific linkage between locus Cm 24 and left ventricular mass index (LVMI). By further expanding that analysis, we detected additional loci that were all linked to LVMI in a sex-specific manner despite their autosomal location. In males, we detected one additional locus (Lvm 8) on Chromosome 5 (LOD=3.4), the two loci Lvm 13 (LOD=4.5) and Lvm 9 (LOD=2.8) on Chromosome 17, and locus Lvm 10 (LOD=4.2) on Chromosome 12. The locus Lvm 13 had the same boundaries as locus Cm 26 previously reported by others using a different cross. None of these loci showed linkage to LVM in females. In contrast, we identified in females the novel locus Lvm 11 on Chromosome 15 (LOD=2.8) and locus Lvm 12 (LOD=2.7) that had the same boundaries on Chromosome 3 as locus Cm 25 detected previously by others using a cross of other normotensive strains. In prepubertal males, there were no differences in the width of cardiomyocytes from WKY and WKHA rats, but cardiomyocytes from WKHA became progressively wider than that of WKY as sexual maturation progressed. Altogether, these results provide evidence that distinct genes may influence LVMI of rats in a sex-dependent manner, maybe by involving sex-specific interactions of sex steroids with particular genes involved in the determination of LVMI and/or cardiomyocyte width.
Animals↗
Experimental evolution of phenotypic plasticity: how predictive are cross-environment genetic correlations?
Genetic correlations are often predictive of correlated responses of one trait to selection on another trait. There are examples, however, in which genetic correlations are not predictive of correlated responses. We examine how well a cross-environment genetic correlation predicts correlated responses to selection and the evolution of phenotypic plasticity in the seed beetle Stator limbatus. This beetle exhibits adaptive plasticity in egg size by laying large eggs on a resistant host and small eggs on a high-quality host. From a half-sib analysis, the cross-environment genetic correlation estimate was large and positive (rA=0.99). However, an artificial-selection experiment on egg size found that the realized genetic correlations were positive but asymmetrical; that is, they depended on both the host on which selection was imposed and the direction of selection. The half-sib estimate poorly predicted the evolution of egg size plasticity; plasticity evolved when selection was imposed on one host but did not evolve when selection was imposed on the other host. We use a simple two-locus additive genetic model to explore the conditions that can generate the observed realized genetic correlation and the observed pattern of plasticity evolution. Our model and experimental results indicate that the ability of genetic correlations to predict correlated responses to selection depends on the underlying genetic architecture producing the genetic correlation.
Animals↗
A mutant strain of Polysphondylium with defects in many genes.
PN6024 is a mutant strain of P. pallidum which appeared on selection for resistance to MDMP, an inhibitor of translation. It was found to be mutant in four other traits, being resistant to tubercidin, incapable of growth at 31.5 degrees C, abnormal in development, and slow growing at 25 degrees C. Genetic crosses using the macrocyst cycle showed that these five traits are controlled by five unlinked genes. The hypothesis is that movement of a transposon to multiple new locations caused these mutations. A difference in restriction fragment pattern between PN6024 and its parent PN600 support the hypothesis. Attempts were made to find conditions generating other strains like PN6024. Selection for growth in the presence of tubercidin yielded clones which resemble PN6024 in being developmentally abnormal as well as tubercidin resistant. Tubercidin treatment also increased the frequency of clones resistant to canavanine. It is suggested that tubercidin is mutagenic because it causes movement of the putative transposon, not because it generates point mutations. Growth under conditions of stress (at 31.5 degrees C, at 8 degrees C, in the presence of 2% ethanol) had at most an erratic effect in generating strains like PN6024. Three substrains appeared spontaneously in cultures of PN6024. These differed in developmental characteristics from each other and from the parent strain. It is suggested that they carry mutations in genes which control the choices between growth and aggregation, and between aggregation and encystment.
Crosses, Genetic↗
KP elements repress P-induced hybrid dysgenesis in Drosophila melanogaster.
Molecular and genetic analysis has revealed a specific P factor deletion derivative (the KP element) which is able to repress P-induced hybrid dysgenesis. All naturally occurring strains lacking the P cytotype (M') that were examined, throughout the world contain up to 30 copies of KP per haploid genome together with complete P factors. The KP element is derived from the P factor by an internal deletion of 1753 bp removing nucleotides 808-2560 and is transcribed to yield an abundant 0.8-kb poly(A)+ RNA with the coding capacity for an in-frame 207 amino acid polypeptide. Genetic crosses show that KP elements preferentially accumulate in the presence of P factors and suppress hybrid dysgenesis. Suppression is transmitted through both sexes and is thus distinct from the maternally transmitted P cytotype mode of suppression. The spread of KP elements is probably due to the continual selection of individuals with the highest numbers of KP elements in which P-induced hybrid dysgenesis is suppressed.
Animals↗
Determinants for stability of the chloroplast psbD RNA are located within its short leader region in Chlamydomonas reinhardtii.
Stability of the chloroplast psbD mRNA encoding the D2 protein of the photosystem II reaction center is drastically decreased in the nuclear photosynthetic mutant nac2-26 of Chlamydomonas reinhardtii. Using biolistic transformation and genetic crosses we have introduced chimeric genes consisting of the psbD leader fused to a reporter gene into the chloroplast in both wild-type and mutant nuclear backgrounds. The chimeric message is destabilized in the latter, but not in the former case, indicating that the 74 nt psbD leader includes one of the target sites for psbD RNA degradation in the absence of wild-type NAC2 function. Increased instability of the psbD leader in mutant versus wild-type chloroplast lysates is also demonstrated in vitro and the primary cleavage sites have been mapped. The instability of the psbD RNA in the mutant correlates with the loss of binding of a 47 kDa protein to the psbD leader RNA, suggesting that this factor acts as message stabilizer in wild-type.
Animals↗
Biochemical and genetic studies of a histidine regulatory mutant of Streptomyces coelicolor A3 (2).
The specific activities of three enzymes in a histidine regulatory mutant RF59 of Streptomyces coelicolor A3(2) resistant to the histidine analogue 1,2,4-triazolealanine (TRA) were measured and compared to the activity of the wild type strain. The first enzyme of the histidine pathway, phosphorybosyl-ATP-pyrophosphorylase (PR-ATP-pyrophosphorylase), of mutant RF59 and the wild type was sensitive to allosteric inhibition by L-histidine and hence feed-back inhibition was not affected by mutation, although the specific activity in the mutant was 2.9 fold higher than in the wild type. The other two enzymes coded by genes from the histidine operon were significantly derepressed. The enzyme D-erythroimidazoleglycerol phosphate dehydrase (IGP-dehydrase) in mutant RF59 had a 4.9 fold higher specific activity than in the wild type strain. The specific activity of the last enzyme of the pathway, histidinol-dehydrogenase (Hol-dehydrogenase), in the mutant was 4.7 fold derepressed compared to the wild type strain. The results of genetic crosses revealed the mapping of RF59 regulatory mutation between argA1 and cysD18 on S. coelicolor chromosome, suggesting that the mutant RF59 is a regulatory mutant unable to fully repress genes of the histidine pathway.
ATP Phosphoribosyltransferase↗
Diploid strains of the pathogenic basidiomycete Cryptococcus neoformans are thermally dimorphic.
Cryptococcus neoformans is an opportunistic human pathogenic fungus with a defined sexual cycle. Clinical and environmental isolates of C. neoformans are haploid, and the diploid stage of the lifecycle is thought to be transient and unstable. In contrast, we find that diploid strains are readily obtained following genetic crosses of congenic MATalpha and MATa strains. At 37 degrees C, the diploid strains grow as yeast cells with a single nucleus that is larger than a haploid nucleus, contains a 2n content of DNA by FACS analysis, and is heterozygous for the MATalpha and MATa loci. At 24 degrees C, these diploid self-fertile strains filament and sporulate, producing recombinant haploid progeny in which meiotic segregation has occurred. In contrast to dikaryotic filament cells that are typically linked by fused clamp connections during mating, self-fertile diploid strains produce monokaryotic filament cells with unfused clamp connections. We also show that these diploid strains can be transformed and sporulated and that an integrated selectable marker segregates in a mendelian fashion. The diploid state could play novel roles in the lifecycle and virulence of the organism and can be exploited for the analysis of essential genes. Finally, the observation that dimorphism is thermally regulated suggests similarities between the lifecycle of C. neoformans and other thermally dimorphic human pathogenic fungi, including Histoplasma capsulatum, Blastomyces dermatitidis, Coccidioides immitis, Paracoccidioides brasiliensis, and Sporothrix schenkii.
Crosses, Genetic↗
Genetic mapping of three GABAA receptor-subunit genes in the mouse.
GABAA receptors are a heterogeneous group of heterooligomeric ligand-gated anion channels that represent the main means of synaptic inhibition in neuronal tissue. At least 14 distinct GABAA subunit proteins representing 5 different classes have been identified. Using rat brain cDNAs for the GABAA receptor beta 1-, alpha 2-, and alpha 4-subunits, we have assigned the corresponding murine genes Gabrb-1, Gabra-2, and Gabra-4 to specific chromosomes with somatic cell hybrids, and we have positioned these genes by analysis of the progeny of three genetic crosses. Gabrb-1 and Gabra-2 are tightly linked on mouse Chromosome 5 between the markers Pgm-1 and Kit, and Gabra-4 maps to proximal mouse Chromosome 7 in apparent proximity to the previously mapped Gabrb-3. The Gabrb-1, Gabra-2 pair of genes on Chr 5 maps near the mouse "circling mutation" pi (pirouette).
Alleles↗
The MEV mouse linkage testing stock: mapping 30 novel proviral insertions and establishment of an improved stock.
Continuing efforts to improve the MEV linkage testing stock are described. The MEV stock carries multiple copies of the ecotropic murine leukemia virus genome. These proviruses are individually detectable in Southern blots, making it possible to follow the segregation of many loci simultaneously in genetic crosses. About 50 novel proviral insertions have been detected in this stock and propagated to homozygosity in a number of sublines. Many of the proviruses were first observed in individuals that were somatic and germinal mosaics. From the minimum frequency of primary transmission of proviruses to offspring, it is estimated that about 7 embryonic cells contribute to the pool of germ cells that populate the gonads. Thirty of the proviruses have been mapped to 15 different chromosomes in intercrosses between MEV sublines and the inbred Mus musculus castaneus strain CAST/Ei or in other crosses. Mapped insertions appear to be randomly distributed among chromosomes, but possibly clustered within chromosomes. Several of the mapped insertions are located such that their inclusion in improved MEV stocks would permit the screening of additional regions of the genome. An improved MEV stock that is homozygous for 12 proviruses on 11 chromosomes, including novel insertions on Chromosomes 17 and 19 is described. The stock also carries four dominant visible markers on 4 additional chromosomes. This stock is estimated to sweep approximately 68% of the autosomal genome.
Alleles↗
A 1.2-Mb YAC contig spans the quaking region.
We describe here a 1.2-Mb yeast artificial chromosome (YAC) contig within the region of mouse chromosome 17 between Brachyury (T) and D17Rp17e, and spanning the quaking (qk) region. We describe six new probes distributed across 1.2 Mb: D17Leh502, D17Leh503, D17Leh504, D17Leh505, D17Leh506, and D17Leh507. Probes D17Leh502 and D17Leh507 are at the extreme ends of the YAC contig. With the exception of D17Leh507, all of these probes are within a deletion associated with the quaking(viable) (qkv) allele of quaking. We have positioned these probes on a detailed YAC physical map together with two previously published probes, D17Leh508 and D17Aus119. We show here that D17Leh508 is also within the qkv deletion. Genetic mapping of D17Leh504 and D17Leh507 on two high-resolution genetic crosses carrying qkv and quaking(lethal-1) (qkl-1) alleles shows that these probes do not recombine with quaking and are therefore within 0.04 cM of qkv and 0.05 cM of qkl-1 mutations. The deletion breakpoint contained within the YAC contig has been positioned to within 90 kb by restriction mapping of wildtype and mutant DNA. This contig will form the basis for identification and mapping of expressed sequences and for an investigation of genome organization.
Alleles↗
Molecular genetic analysis of distal mouse chromosome 6 defines gene order and positions of the deafwaddler and opisthotonos mutations.
Two neurological mutants deafwaddler (dfw) and opisthotonos (opt) and a cluster of three Shaker-like potassium (K) channel genes Kcna1, Kcna5, and Kcna6 were all independently mapped to distal mouse chromosome six (Chr 6). In this study, genetic and molecular techniques were employed to assess directly the linkage of the two mutants and to investigate the likelihood that a mutation in one of the three K channel genes may underlie dfw and/or opt. Genetic crosses testing for allelism showed that the dfw and opt mutations complement each other. Additional crosses demonstrated that the mutants are separated by a recombination distance of 3.1 +/- 1.8 cM. Microsatellite marker analysis of the crossover chromosomes recovered from the opt, dfw recombination study indicated that opt maps centromeric to dfw. The location of the K channel genes relative to the dfw mutation was determined by mapping these genes and 15 microsatellite markers in an intersubspecific backcross (IB) segregating for dfw [(CAST/Ei-+/+ x C3HeB/FeJ-dfw/dfw) x C3HeB/FeJ-dfw/dfw]. Analysis of the backcross progeny positioned the dfw locus in the interval between the microsatellite markers D6Mit11 and D6Mit55, D6Mit63. The K channel cluster maps telomeric to dfw. This study establishes the gene order cen-opt-dfw-Rho (D6Mit44)-Kcna1, Kcna5, Kcna6 on distal mouse Chr 6 and suggests that the neurological mutants opt and dfw affect two different genes, neither of which is caused by a mutation in any one of the three clustered K channels.
Animals↗
Genetic mapping with dispersed repeated sequences in the rice blast fungus: mapping the SMO locus.
The SMO genetic locus in strains of the fungus Magnaporthe grisea that infect weeping lovegrass, directs the formation of correct cell shapes in asexual spores, infection structures, and asci. We have identified and characterized a Smo- strain of M. grisea that infects rice. The smo mutation in this strain segregates as a single gene mutation and is allelic to previously identified smo alleles. A marked reduction in pathogenicity co-segregates with the Smo- phenotype, suggesting that the SMO locus plays a role in rice pathogenicity. A family of dispersed repeated DNA sequences, called MGR, have been discovered in the nuclear DNA of M. grisea rice pathogens. Genetic crosses between Smo- rice pathogens and Smo+ non-rice pathogens were used to follow the segregation of the SMO locus and individual MGR sequences. Using DNA blot analysis with cloned MGR hybridization probes, we mapped the SMO locus to a chromosomal region flanked by two closely linked MGR sequences. We demonstrated that the copy number of MGR sequences could be reduced in subsequent crosses to non-rice pathogens of M. grisea, and that new MGR sequences did not occur following meiosis indicating that these sequences are stable in the genome. We conclude that restriction fragment polymorphism mapping with cloned MGR sequences as hybridization probes is an effective way to map genes in the rice blast fungus.
Ascomycota↗