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Assignment of the gene for adenine phosphoribosyltransferase on the genetic map of mouse chromosome 8.

Two electrophoretic variants of adenine phosphoribosyltransferase (APRT) were identified in a population of wild mice (Mus musculus bactrianus). Breeding tests demonstrated that the APRT variants are under the control of two alleles at an autosomal locus designated Aprt. We have examined the linkage relationships between Aprt and the markers of chromosome 8 including esterase-1 and the centromere. The recombination distance between the centromere and Aprt is 44 +/- 7 cM, and that between Es-1 and Aprt is 25 +/- 2 cM, i.e., the probable order of the markers examined is cen-Es-1-Aprt on chromosome 8.

Adenine Phosphoribosyltransferase↗

Genetic mapping of four DNA markers (DXS16, DXS43, DXS85, and DXS143) from the p22 region of the human X chromosome.

Linkage analysis of four polymorphic anonymous DNA markers from the Xp22 region was performed using families from the Centre d'Etude du Polymorphisme Humain. The loci DXS43 (pD2) and DXS16 (pXUT23) were found to be tightly linked (theta = 0.02 at Z = 14.96) and proximal to both DXS85 (782) and DXS143 (dic56). Multipoint linkage analysis suggests the order: (Formula: see text).

Alleles↗

Genetic mapping and protein product diversity of the self-incompatibility locus in wild tomato (Lycopersicon peruvianum).

Phenotypic diversity of self-incompatibility (S) alleles within nine natural populations of Lycopersicon peruvianum was investigated. Only 7 incompatible responses were observed of a total of 276 unique combinations tested, on the basis of controlled pollinations, indicating the large number of alleles that exist within these populations. Molecular weight polymorphism for specific major stylar proteins observed on SDS-PAGE was also evident in two of the populations examined. Five proteins were shown to map to the S locus and to be associated with different S alleles through controlled pollinations and segregation of the proteins. Two of these S related proteins had been described previously in terms of spatial and temporal expression consistent with their involvement in self-incompatibility (Mau et al., Planta 169, 184-191, 1986). A mapping population derived from a fully compatible cross was used to establish linkage of the S locus to two DNA markers, CD15 and TG184, that lie on chromosome 1. The order of the markers and estimates of map distances are given.

Alleles↗

Genetic mapping of the t-complex region on mouse chromosome 17 including the Hybrid sterility-1 gene.

t-haplotypes occupy a region on chromosome (Chr) 17 which slightly overlaps the ends of the T-H-2 interval. The wild-type form of this 14 centi-Morgan (cM) region was mapped in a multilocus backcross (C57BL/10-T x C3H)F1 x C57BL/10 using 15 DNA probes on Southern blots of the DNA extracted from 53 animals which were recombinants in the T-H-2 interval. Each recombinant was also progeny-tested to ascertain its Hybrid sterility-1 (Hst-1) genotype by crossing to PWB/Ph, a Mus musculus-derived inbred strain. The limit of resolution of the cross was 0.27 cM. The map distances have been determined for the DNA loci in the T-H-2 interval and the Hst-1 gene was mapped in close vicinity to the D17Rp17 locus.

Animals↗

Genetic mapping of the gene affecting polyphenol oxidase activity in tetraploid durum wheat.

The quality of durum wheat (Triticum turgidum ssp. durum) is influenced by polyphenol oxidase(PPO) activity and its corresponding substrates. A saturated molecular-marker linkage map was constructed previously by using a set of recombinant inbred (RI) lines, derived from a cross between durum wheat cultivars Jennah Khetifa and Cham 1. Quantitative trait loci (QTL) for PPO activity in seeds were mapped in this population. PPO activity in seeds of the parents and 110 RI lines was measured spectrophotometrically. The PPO activity of Cham 1 was significantly lower than that of Jennah Khetifa. QTL analysis of these data indicated that most of PPO activity was associated with major loci on the long arm of chromosome 2A. The trait was found to be strongly associated with the SSR marker Xgwm312@2A. With this knowledge, marker-assisted selection can be used to select genotypes with lower PPO activity in durum wheat populations.

Breeding↗

Fine genetic mapping of the TuNI locus causing systemic veinal necrosis by turnip mosaic virus infection in Arabidopsis thaliana.

In the pathosystem of turnip mosaic virus (TuMV) and Arabidopsis thaliana, two distinct symptoms (mosaic symptom and veinal necrosis) were observed that were dependent upon the combination of the TuMV isolate and the Arabidopsis ecotype. The Col-0 ecotype developed mosaic symptoms after infection with the TuMV isolate Azu while the Ler ecotype developed veinal necrosis after infection with the same TuMV isolate. The Ler phenotype is controlled by a single dominant gene TuNI (TuMV necrosis inducer) which is located on chromosome 1. The TuNI gene was precisely mapped to the ~105 kb interval between the two markers of mXF41 and mRF28 by using several types of DNA polymorphism markers. Within this region, which included largely duplicated sequences, a total of 19 putative genes were predicted and 15 of these were classified into five gene families. The genes belonging to the gene families At1g58480 and At1g58602 may function in response to infection by pathogens. The gene family At1g58480 encodes lipase-like proteins, which might be involved in the induction of defence responses that are mediated by salicylic acid. The gene family At1g58602 encodes the CC-NBS-LRR (CNL) proteins, which are known to function as one of the plant resistance (R) proteins against pathogens. In the present study, the possibility that TuNI might function as an R gene was discussed.

Arabidopsis↗

Genetic mapping of maize stripe disease resistance from the Mascarene source.

Maize stripe virus (MStV) is a potentially threatening virus disease of maize in the tropics. We mapped quantitative trait loci (QTLs) controlling resistance to MStV in a maize population of 157 F(2:3) families derived from the cross between two maize lines, Rev81 (tropical resistant) and B73 (temperate susceptible). Resistance was evaluated under artificial inoculations in replicated screenhouse trials across different seasons in Réunion Island, France. Composite interval mapping was employed for QTL detection with a linkage map of 143 microsatellite markers. Heritability estimates across seasons were 0.96 and 0.90 for incidence and severity, respectively, demonstrating a high genotypic variability and a good control of the environment. Three regions on chromosomes 2L, 3 and 5, with major effects, and another region on chromosome 2S, with minor effects, provided resistance to MStV in Rev81. In individual seasons, the chr2L QTL explained 60-65% of the phenotypic variation for disease incidence and 21-42% for severity. The chr3 QTL, mainly associated with incidence and located near centromere, explained 42-57% of the phenotypic variation, whereas the chr5 QTL, mainly associated with severity, explained 26-53%. Overall, these QTLs explained 68-73% of the phenotypic variance for incidence and 50-59% for severity. The major QTLs on chr2 and 3 showed additive gene action and were found to be stable over time and across seasons. They also were found to be included in genomic regions with important clusters of resistance genes to diseases and pests. The major QTL on chr5 appeared to be partially dominant in favour of resistance. It was stable over time but showed highly significant QTL x season interactions. Possible implications of these QTLs in different mechanisms of resistance against the virus or the insect vector are discussed. The prospects for transferring these QTLs in susceptible maize cultivars and combining them with other resistances to virus diseases by conventional or marker-assisted breeding are promising.

Chromosome Mapping↗

Characterization and genetic mapping of phosphoglucoisomerase mutations in mannitol-negative mutants of Pseudomonas aeruginosa.

Phosphoglucoisomerase (pgi) mutations in a number of independently isolated mannitol-negative mutants of Pseudomonas aeruginosa PAO1 were mapped on the chromosome by plasmid FP5-mediated conjugation and by cotransduction with the generalized transducing phages G101 and F116L. Mutant allele pgi-9001 exhibited linkage to ilvB, C-9059 (46-85%), car-9003 (93-100%), and pur-9047 (70%), but not with met-9011, in FP5-mediated conjugational crosses. All known pgi mutations and several previously uncharacterized mannitol-negative mutations exhibited transductional linkage to two independent car mutations at frequencies ranging from 13% to 42% and 53% to 99%, in transductional crosses mediated by phages G101 and F116L respectively. These pgi and mannitol-negative mutations also were cotransducible at very low frequencies (<1%) with two independent ilv mutations. Cotransduction of the car and ilv loci could not be detected. These data suggest the location of pgi within the first minute of the P. aeruginosa chromosome closely linked to the car marker and probably between the ilv and car loci. All of the mannitol-negative mutations that exhibited linkage to the car and ilv loci were characterized as pgi mutations by enzyme assays. A phenotypically similar, mannitol-negative mutant was shown to contain a mutation in glucose-6-phosphate dehydrogenase (zwf-9012) that maps to a different region on the chromosome.

Chromosome Mapping↗

High-resolution genetic mapping of the saccharin preference locus (Sac) and the putative sweet taste receptor (T1R1) gene (Gpr70) to mouse distal Chromosome 4.

The Sac (saccharin preference) locus affecting mouse behavioral and neural responsiveness to sweeteners has been mapped to distal Chr 4. A putative sweet taste receptor, T1R1, has been recently cloned, and the gene encoding it, Gpr70, has also been mapped to mouse distal Chr 4. To assess Gpr70 as a candidate gene for Sac, we compared the Gpr70 sequences of C57BL/6ByJ and 129P3/J mouse strains with different alleles of Sac. Using Gpr70 sequence variation between the C57BL/6ByJ and 129P3/J strains, we conducted a high-resolution analysis of the chromosomal localization of the Gpr70 and Sac loci in the F2 hybrids and 129.B6-Sac partially congenic mice originating from these two strains. The Gpr70 gene maps proximal to Sac, which demonstrates that they are different loci.

Animals↗