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Results for “Genes, Recessive”

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At least 91 records · Page 5Linked to original sources
PubMed2003

SNP-based codominant markers for a recessive gene conferring resistance to corky root rot (Rhizomonas suberifaciens) in lettuce (Lactuca sativa).

The analysis of F2 progeny and derived F3 families of Lactuca sativa segregating for resistance to corky root rot caused by Rhizomonas suberifaciens permitted the identification of restriction fragment length polymorphism (RFLP) and single nucleotide polymorphism (SNP) markers linked to the recessive resistance gene cor. PCR-based markers were identified by bulked segregant analysis (BSA). Allele-specific primers were generally designed with the 3 terminal base coinciding with an SNP, matching one of the alleles and mismatching the other, and with an additional subterminal 3 base mismatching both alleles. Codominant, robust, and inexpensive molecular markers were obtained that used standardized PCR conditions. Some of the markers could be analyzed in multiple Lactuca mapping populations that did not segregate for disease resistance allowing the cor locus to be located on several maps. The consistent low density of markers around cor in these maps suggests that cor may be in an area with an elevated rate of recombination. Evaluation of these markers in a large sample of cultivars and landraces identified pairs of flanking polymorphic markers that can be used for marker-assisted selection of corky root resistance.

Chromosome Mapping↗
PubMed1992

Schistosoma mansoni: hycanthone/oxamniquine resistance is controlled by a single autosomal recessive gene.

Individual schistosomes of an hycanthone/oxamniquine-sensitive strain were crossed with individual schistosomes of the opposite sex and belonging either to the same sensitive population or to a different strain which exhibited high resistance to the two drugs. Schistosome crosses were performed by transfer of single worm pairs into the mesenteric veins of mice and the drug sensitivity/resistance of individual progeny worms was assessed using an in vitro test. Drug resistance behaved as an autosomal recessive trait, as shown by the results of the F1 and F2 generation and of the backcrosses. Drug-resistant worms appeared to be slightly less viable than their sensitive counterpart at all stages of the life cycle. The results are relevant for an interpretation of drug resistance and drug mechanisms and the approach used in this study may be applicable to different genetic markers in schistosomes.

Animals↗
PubMedDate not supplied

Inheritance of resistance to clopyralid and picloram in yellow starthistle (Centaurea solstitialis L.) is controlled by a single nuclear recessive gene.

The noxious weed yellow starthistle (Centaurea solstitialis L.) can be controlled effectively at the seedling stage with foliar application of the auxinic herbicides picloram or clopyralid. Although resistance to these herbicides is rare, a yellow starthistle biotype resistant to picloram and cross-resistant to clopyralid was observed in 1989 near Dayton, WA, in a pasture that had been subjected to intensive picloram selective pressure. Our objective was to determine the mode of inheritance for this resistance trait. Transmission of the resistant phenotype was monitored in reciprocal F(1) crosses between susceptible (SCI) and resistant (RDW) plants, their testcross and pseudo-F(2) progeny. Progeny from all crosses, as well as RDW and SCI seedlings of original populations, were sprayed with picloram or clopyralid to distinguish between susceptible and resistant individuals. All F(1) progeny were susceptible to both herbicides, indicating that the resistance trait was of nuclear origin and recessive in nature. Segregation of the resistant phenotype among pseudo-F(2) and testcross progeny of F(1) genotypes demonstrated monofactorial inheritance (P >.25) for resistance to both herbicides. The conclusion that resistance is conferred by a single recessive allele is consistent with the observation that no other picloram-resistant yellow starthistle populations have been identified in the area since picloram selection pressure was abated.

Centaurea↗
PubMed1990

Specific recognition of human CD3-CD16+ natural killer cells requires the expression of an autosomic recessive gene on target cells.

We analyzed the recently defined ability of CD3-CD16+ cells to specifically recognize and lyse normal allogeneic target cells (PHA-induced blasts). The susceptibility to lysis by a given alloreactive natural killer (NK) clone ("1 anti-A") was expressed by PHA blasts derived from 9 of 38 random donors analyzed. In all instances, the specific lysis of "susceptible" target cells was greater than 35% while that of "nonsusceptible" targets was less than 6% at an E/T cell ratio of 5:1. In addition to 1 anti-A, A anti-1 specific CD3-CD16+ clones could also be isolated from the reverse MLC combination. The relationship existing between lysis of normal allogeneic cells or tumor cells by the same CD3-CD16+ effector cell has been investigated: 1 anti-A specific CD3-CD16+ clones lysed PHA blasts of three of six cancer patients, while they lysed fresh tumor cells (ovarian carcinoma) from all six patients. The type of inheritance of the character "susceptibility to lysis" was analyzed in representative families. This analysis revealed that the character is inherited in an autosomic recessive fashion, and it is therefore different from MHC. We further investigated the type of segregation of the opposite character "resistance to lysis" (which is inherited in a dominant mode). The finding that this character segregated in all donors expressing given MHC haplotypes indicated that the gene regulating the expression of the NK-defined alloantigen is present on chromosome 6.

Antibodies, Monoclonal↗
PubMed2002

Fetal anasarca (Hydrops foetalis) associated with lymphoid tissue agenesis possibly due to an autosomal recessive gene defect in sheep.

Fourteen hydrops fetalis cases appeared in a sheep flock in the Soria province of Central Spain in two lambing seasons in 2000. There were no previous cases of hydrops fetalis in this flock. Normal delivery could not be completed because fetal weights ranged from 12 to 16 kg and fetuses had massive subcutaneous edema. Five affected pregnant females were studied. The complete lack of lymph nodes in the fetuses was the most outstanding finding, this anomaly likely being the origin of generalized fluid accumulation. Karyotypes were normal. A blind protocol of parentage testing was performed by means of DNA microsatellite analysis, and one of the five existing rams was found to be the only compatible sire of the affected fetuses. This male had been selected from the same flock while the other rams had all been acquired from other farms. The first cases appeared when this ram began breeding, and no cases were observed after replacing it. Male and female fetuses were affected in similar proportions. The existence of a recessive allele affecting normal lymph node embryonic development in this flock is proposed as the most appropriate hypothesis. As a consequence, the use of rams from different farms is indicated as an efficient emergency measure in similar situations, while the affected flock should be excluded from selection programs as long as the anomalous gene remains unidentified.

Animals↗
PubMed2004

Identification of markers tightly linked to sbm recessive genes for resistance to Pea seed-borne mosaic virus.

Two virus resistance loci on linkage groups II and VI have provided the only sources of natural resistance against Pea seed-borne mosaic virus (PSbMV, Potyviridae) in the important crop plant Pisum sativum L. A combination of parallel approaches was used to collate linked markers, particularly for sbm-1 resistance on linkage group VI. We have identified sequences derived from the genes for the eukaryotic translation initiation factors eIF4E and eIF(iso)4E as being very tightly linked to the resistance gene clusters on linkage groups VI and II, respectively. In particular, no recombinants between sbm-1 and eIF4E were found amongst 500 individuals of an F2 cross between the BC4 resistant line (JI1405) and its recurrent susceptible parent 'Scout'. In a different mapping population, the gene eIF(iso)4E was also shown to be linked to sbm-2 on linkage group II. A parallel cDNA-AFLP comparison of pairs of resistant and susceptible lines also identified an expressed tag marker just 0.7 cM from sbm-1. eIF4E and eIF(iso)4E have been associated with resistance to related viruses in other hosts. This correlation strengthens the use of our markers as valuable tools to assist in breeding multiple virus resistances into peas, and identifies potential targets for resistance gene identification in pea.

Agriculture↗
PubMed1983

Patient with 13 chromosome deletion: evidence that the retinoblastoma gene is a recessive cancer gene.

Although a constitutional chromosomal deletion including 13q14 has been found to date in all retinoblastoma patients whose esterase D activity is 50 percent of normal, one female patient has been found who has 50 percent esterase D activity in all normal cells examined but no deletion of 13q14 at the 550-band level. Therefore, she has the smallest constitutional chromosomal deletion within 13q14 that is associated with susceptibility to retinoblastoma. Two stem lines were identified in a retinoblastoma from this patient, and each one had a missing 13 chromosome. No detectable esterase D activity was found in the tumor, indicating that the normal nondeleted 13 chromosome was lost in both stem lines. Thus the data from this patient not only show that there is a total loss of genetic information at the location of the retinoblastoma gene within the tumor, but also imply that recessive genes may play an important role in the development of certain human tumors including retinoblastoma.

Child, Preschool↗
PubMed1991

A cultivar-specific interaction between Rhizobium leguminosarum bv. trifolii and subterranean clover is controlled by nodM, other bacterial cultivar specificity genes, and a single recessive host gene.

Insertion mutagenesis identified two negatively acting gene loci which restrict the ability of Rhizobium leguminosarum bv. trifolii TA1 to infect the homologous host Trifolium subterraneum cv. Woogenellup. One locus was confirmed by DNA sequence analysis as the nodM gene, while the other locus, designated csn-1 (cultivar-specific nodulation), is not located on the symbiosis plasmid. The presence of these cultivar specificity loci could be suppressed by the introduction of the nodT gene from ANU843, a related R. leguminosarum bv. trifolii strain. Other nod genes, present in R. leguminosarum bv. viciae (including nodX) and R. meliloti, were capable of complementing R. leguminosarum bv. trifolii TA1 for nodulation on cultivar Woogenellup. Nodulation studies conducted with F2 seedlings from a cross between cultivar Geraldton and cultivar Woogenellup indicated that a single recessive gene, designated rwt1, is responsible for the Nod- association between strain TA1 and cultivar Woogenellup. Parallels can be drawn between this association and gene-for-gene systems common in interactions between plants and biotrophic pathogens.

Bacterial Proteins↗
PubMed1999

A gene for autosomal recessive symmetrical spastic cerebral palsy maps to chromosome 2q24-25.

Cerebral palsy has an incidence of approximately 1/500 births, although this varies between different ethnic groups. Genetic forms of the disease account for approximately 1%-2% of cases in most countries but contribute a larger proportion in populations with extensive inbreeding. We have clinically characterized consanguineous families with multiple children affected by symmetrical spastic cerebral palsy, to locate recessive genes responsible for this condition. The eight families studied were identified from databases of patients in different regions of the United Kingdom. After ascertainment and clinical assessment, we performed a genomewide search for linkage, using 290 polymorphic DNA markers. In three families, a region of homozygosity at chromosome 2q24-q25 was identified between the markers D2S124 and D2S148. The largest family gave a maximum LOD score of 3.0, by multipoint analysis (HOMOZ). The maximum combined multipoint LOD score for the three families was 5.75. The minimum region of homozygosity is approximately 5 cM between the markers D2S124 and D2S2284. We have shown that a proportion of autosomal recessive symmetrical spastic cerebral palsy maps to chromosome 2q24-25. The identification of genes involved in the etiology of cerebral palsy may lead to improved management of this clinically intractable condition.

Adolescent↗
PubMed1986

Somatic events unmask recessive cancer genes to initiate malignancy.

A heritable mutation predisposes an individual to certain childhood malignancies, such as retinoblastoma and Wilms' tumor. The chromosomal locations of the genes responsible for the predisposition are known by linkage with chromosomal deletions and enzyme markers. A study of these tumors in comparison to the normal constitutional cells of the patients, using enzyme and DNA markers near the predisposing genes, has shown that these genes are recessive to normal wild-type alleles at the cellular level. Expression of the recessive phenotype (malignancy) involves the same genetic events that were observed in Chinese hamster cell hybrids carrying recessive drug resistance genes. In both the experimental and clinical situations, the wild-type allele is most commonly eliminated by chromosome loss with duplication of the mutant chromosome. Simple chromosome loss and mitotic recombination have been documented in both systems. In the remaining 30% of cases, inactivation or microdeletion of the wild-type allele are assumed to be responsible for expression of the recessive phenotype. Osteosarcoma is a common second tumor in patients who have had retinoblastoma. Studies with markers in osteosarcoma show that these tumors also result from unmasking of the recessive phenotype by loss of the normal allele at the retinoblastoma locus, whether or not the patient had retinoblastoma. Subsequent chromosomal rearrangements and amplification of oncogenes that occur in these homozygous tumors provide progressive growth advantage. In other malignancies, in which studies have so far focused on oncogene amplification and chromosomal rearrangements, unmasking of recessive mutations may also be the critical initiating events.

Animals↗
PubMed1986

The NOD mouse: recessive diabetogenic gene in the major histocompatibility complex.

Examination of the histocompatibility region of the nonobese diabetic (NOD) mouse with antibodies against class II glycoproteins (products of immune response genes of the major histocompatibility complex I-A and I-E), hybrid T-cell clones, and mixed-lymphocyte cultures and analysis of restriction fragment length polymorphisms indicate that the NOD mouse has a unique class II major histocompatibility complex with no expression of surface I-E, no messenger RNA for I-E alpha, and an I-A not recognized by any monoclonal antibodies or hybrid T-cell clones studied. In crosses of NOD mice with control C3H mice, the development of diabetes was dependent on homozygosity for the NOD mouse's unique major histocompatibility region.

Animals↗
PubMed1989

A recessive tumor gene function in Drosophila is involved in cell adhesion.

The phenotypic effects of lethal (2) giant larvae mutations are due to unstructured growth of brain and imaginal disc cells in homozygous mutant larvae. Molecular properties of the wildtype l (2) gl protein and its tissue specificity of expression suggest that the protein is required for the adhesion of cells which are about the stop cell division and undergo terminal differentiation.

Animals↗