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At least 19 recordsLinked to original sources
PubMed1979

Dysgenetic lens (dyl)--a new gene in the mouse.

A new autosomal recessive gene, dysgenetic lens (dyl), in the mouse is described. Homozygotes are fully viable and exhibit smaller eye, corneal opacity, adhesion of the iris, cataractous degeneration, and extrusion of the lens nucleus and persistent lens-epithelium attachment. Developmental failure of lens vesicle--ectoderm separation is recognized as the earliest expression of the genetic defect. Possible significance of this mutant in the understanding of Peter's anomaly is indicated.

Animals↗
PubMed1976

New gene locus modifying susceptibility to certain B-tropic murine leukemia viruses.

A new gene, SRV, the dominant allele of which occurs in mice of strain C57BL, independently modifies the slope ("hitness") and level of sensitivity of the titration curves obtained when one subclass of B-tropic murine leukemia viruses is propagated on mouse embryo cells of nonpermissive Fv-1 genotypes. Replication of another subclass of B-tropic viruses is not modified with respect to hitness, and that of N-tropic viruses is not affected.

Animals↗
PubMed1979

A new gene involved in expression of fructose-1,6-diphosphate aldolase activity in Escherichia coli.

A new gene, fdaB, has been mapped by transduction and partial diploid analyses and located adjacent to argA at 59.9 min on the Escherichia coli recalibrated linkage map. This gene is involved in expression of fructose-1,6-diphosphate aldolase activity and indirectly in ribosomal RNA synthesis. The temperature-sensitive mutant strain AA-157, containing the defective gene product of of fdaB, accumulates high concentrations of fructose 1,6-diphosphate at the nonpermissive temperature.

Chromosome Mapping↗
PubMed2026

Searching for New Genes That Cause Usher Syndrome.

PURPOSE: The purpose of this project was to identify novel Usher syndrome (USH) candidate genes from phenotyping data of 9139 knockout (KO) mouse lines. METHODS: We evaluated phenotype data for concurrent retinopathy and hearing abnormalities in single-gene KO mice generated by the International Mouse Phenotyping Consortium (IMPC). A search was performed to determine whether each gene had been previously associated with retinopathy and/or deafness in humans. Bioinformatic tools were used to predict protein interactions, molecular functions, signaling pathways, and the expression of human orthologues of candidate genes in the retina and inner ear. RESULTS: We identified 18 single-gene KO lines exhibiting hearing abnormality and retinopathy after ear and eye examinations, respectively, and/or by histopathology. The molecular functions and signaling pathways of the human orthologues of the 18 candidate genes partially overlapped with those of USH genes. Particularly, FER and DYRK1B proteins were predicted to interact with proteins encoded by known ciliopathy genes. ADIPOR1, ATP8B1, and MPDZ were associated with retinal degeneration in humans. CHSY1 and IDUA may be pathogenic causes of hearing impairment in people. Furthermore, CHSY1, CSTB, and SPRED1 were located adjacent to unsolved genetic loci related to USH. CONCLUSIONS: A screen of 9139 KO mouse lines revealed 18 candidate genes exhibiting both retinal and inner ear abnormalities consistent with the principal clinical features associated with USH. As the observed phenotypes are attributed to gene deletion in mice, these genes warrant further study to determine the causation of retinal degeneration and hearing loss in patients.

Animals↗
PubMed1979

New genes and promoters suggested by the DNA sequence near the end of the coliphage T7 early operon.

We have employed the dideoxynucleotide chain-terminating method to determine the nucleotide sequence of T7 DNA between the physical map positions 18.9% and 19.8%. The most striking features of this sequence are two perfect 21-basepair repeats, each of which appears to contain a promoter for late transcription. In each case the promoter sequence incorporates a putative translational terminator on its left (5'-side of the "sense" strand), and overlaps a potential ribosome-binding site on its right. The region probably lies immediately distal to the early operon, and may contain two short, hitherto unreported protein-coding sequences.

Base Sequence↗
PubMed1979

A new gene of Escherichia coli K-12 whose product participates in T4 bacteriophage late gene expression: interaction of lit with the T4-induced polynucleotide 5'-kinase 3'-phosphatase.

We isolated five Escherichia coli mutants deficient in their ability to support the late (replication-coupled) gene expression of T4 bacteriophage at 30 degrees C. These mutants, which we call Lit mutants, define at least one novel gene at 25 min on the E. coli map. They were selected in an attempt to obtain mutants which restrict the growth of T4 mutants deficient in polynucleotide 5'-kinase 3'-phosphatase but not that of wild-type T4 at 37 degrees C. Some of the mutants do have these phenotypes under some conditions. Studies of the block in T4 development in some of the E. coli mutants suggest that Lit mutants are affected in a gene product involved in the metabolism of deoxyribonucleic acid nicks or single-strand gaps. None of the Lit mutants is deficient in the major, bacterial, 3'-phosphatase activity in crude extracts.

Chromosome Mapping↗
PubMed2025

Functional genetics of rice PISTILLATA genes reveals new roles and target genes in flowering time, female fertility, and parthenocarpy.

Floral organ identity is controlled largely by the combinatorial action of MADS domain homeotic transcription factors. Lodicules are specialized plant organs in cereals and grasses that are involved in floret opening and facilitate pollination and fertility in rice (Oryza sativa L.). To understand the mechanisms underlying the specification of the rice lodicule, we investigated the developmental functions of the rice PISTILLATA (PI) paralogs, OsMADS2, and OsMADS4. Null osmads2 mutants reiterated OsMADS2 nonredundant lodicule specification roles and revealed new roles in flowering time and floral organ number and fate. Doubly perturbed osmads2 osmads4kd florets had severe abnormalities, were female infertile, yet could initiate parthenocarpy. Ubiquitous OsMADS4 overexpression rescued osmads2 abnormalities. We also utilized genome-wide binding analyses and transcriptome profiling to identify putative target genes contributing to OsMADS2 functions. In osmads2d8/d8 null mutant, we observed deregulated genes in a plethora of processes including lodicule and stamen development, floral organ number, and cell wall development. Some examples are cell division regulators (Cyclin D6, Cyclin-P4-1-like), an aquaporin (PIP1A), a peptide transporter, a vascular developmental regulator (HOX1), and a cell wall modulator (GH9B16). The deregulation of these genes may be associated with the disrupted cell division, tissue differentiation, and physiology of the malformed lodicules in osmads2 and osmads2 osmads4kd florets. Altogether, we reveal novel roles for the rice PI paralogs in flowering time, panicle exsertion, and embryo sac differentiation, identify gene targets for lodicule development, and provide mechanistic insights on the functional diversification of rice PI paralogs.

Oryza↗
PubMed1979

Tail anomaly lethal Tal: a new mutant gene in the rat.

A new hereditary tail anomaly (gene symbol Tal) in rats was found in the course of teratological studies with trypan blue. The characteristic feature of the tail anomaly was a short and kinked tail. The genetic analysis indicated that the tail anomaly was caused by an autosomal dominant gene and the homozygotes were lethal in the prenatal stage. The first sign of degeneration in the homozygous embryo appeared in the late egg cylinder stage. The phenotype of this mutant is similar to that of T-locus mutants in mice.

Abnormalities, Drug-Induced↗
PubMed1979

Use of two-dimensional electrophoresis to identify and map new mouse genes.

Cytosol polypeptides from mouse liver have been examined using two-dimensional electrophoresis. About 250 spots were readily discernible. When cytosols from strains BALB/cBy and C57BL/6By were compared eight genetically determined differences were observed. Other strain pairs show comparable numbers of differences. These eight phenotypes were scored in seven recombinant inbred lines derived from the two parental strains, and their strain distribution patterns were compared with previously determined patterns for other genetic markers that differ between the two progenitor strains. Using this information, tentative chromosomes assignments for the genes controlling five of the variant phenotypes have been made, and two of the assignments have been confirmed using congenic resistant strains. These eight genes will be useful reference markers in future crosses designed to map new genes.

Animals↗
PubMed1979

Mapping of a new hem gene in Escherichia coli K12.

A new type of haem-deficient mutant was isolated in Escherichia coli K12 by neomycin selection. The mutant, designated SASX38, accumulated uroporphyrin, coproporphyrin and protoporphyrin. Since it possessed normal ferrochelatase activity, it was assumed to be deficient in protoporphyrinogen oxidase activity. The gene affected in the mutant was designated hemG. Mapping of the hemG gene by phage P1-mediated transduction showed that it was located very close to the chlB gene (frequency of cotransduction 78.7%), between the metE and rha markers. This location is distinct from the other known hem loci in E. coli K12.

Chromosome Mapping↗
PubMedDate not supplied

Evidence for a new lethal gene causing cardiomyopathy in Japanese black calves.

Sudden death with severe dyspnea in new-born or infant calves confined to a family of Japanese black cattle was studied. Neither environmental nor bacteriological factors seemed to be involved in the etiology of the disease. Histopathological examination revealed focal degeneration and necrosis of the muscle fibers in the myocardium, to which a diagnosis of idiopathic cardiomyopathy was proposed. The pedigree and mating type analyses suggested that a new autosomal recessive lethal gene was responsible for the syndrome. Rates of incidence of the affected calves in five sire families were tested for an expectation of 12.5 percent incidence by the chi-square method.

Animals↗
PubMedDate not supplied

Specific immune response genes of new inbred strains of guinea pigs.

Distribution of specific immune-response (Ir) genes controlling responsiveness to synthetic polypeptide antigens, homopolymer of poly-L-lysine (PLL), copolymer of L-glutamic acid and L-alanine (GA) and copolymer of L-glutamic acid and L-tyrosine (GT), and limiting doses of 2,4-dinitrophenyl guinea pig serum albumin (DNP-GPA) was surveyed in new inbred strains of guinea pigs, JY 1, JY 2, JY 9 and JY 10, established in this Institute. The PLL gene was not found in any of the guinea pigs. The GA gene was found in JY 1 and JY 2 guinea pigs and the GT gene in all the guinea pigs. The gene controlling responsiveness to low doses (1 microgram) of DNP-GPA was found in JY 1, JY 9 and JY 10 guinea pigs. The associated (Ia) antigens was discussed.

Animals↗