scholarly journals IDENTIFICATION OF AN AUTOSOMAL LOCUS AFFECTING STEROID SULFATASE ACTIVITY AMONG INBRED STRAINS OF MICE

Genetics ◽  
1983 ◽  
Vol 105 (1) ◽  
pp. 181-189
Author(s):  
Robert P Erickson ◽  
Kenneth Harper ◽  
James M Kramer

ABSTRACT We have found an activity variant for testicular and liver steroid sulfatase among inbred strains of mice that is not X-linked. C57BL/6J, SM/J and SWR/J testicular extracts hydrolyze 3H-dehydroepiandrosterone sulfate twice as rapidly as do A/J extracts. The C3H/HeJ and DBA/2J strains were intermediate. The Km values for C57BL/6J and A/J are 2.29 ± 0.10 and 1.01 ± 0.02 μM, respectively. The F1 values in both directions were intermediate, which argues against X-linkage of this trait. F2 values show scattered high-intermediate-low values compatible with assay variation superimposed on the segregation of codominant alleles. When assayed for both testicular and liver steroid sulfatase, nine recombinant inbred lines between A/J and C57BL/6J segregate to near the parental strain values. Thus, this activity variation for steroid sulfatase appears to be determined by a single gene, which is not X-linked. Sex and steroidal hormone differences in liver steroid sulfatase activity were not present in the A/J strain, but females of the C57BL/6J and some recombinant inbred lines had higher levels. Electrophoretic studies only disclosed a variant in the SM/J strain, which seems to be secondary to the well-known neuraminidase variation in SM/J.

1983 ◽  
Vol 42 (2) ◽  
pp. 159-168 ◽  
Author(s):  
Jasna Markovac ◽  
Robert P. Erickson

SUMMARYGenetic variation in the amount of binding of dihydroalprenolol (a potent antagonist) to hepatocyte β-adrenergic receptors has been observed among inbred strains of mice. This variation is attributed to a differential effect of magnesium on the receptors between the high and low binding strains. Evidence for a single gene controlling the magnesium effect on dihydroalprenolol binding to β-adrenergic receptors was found using recombinant inbred lines between the high and low strains. We suggest the provisional gene symbol Badm.


1986 ◽  
Vol 164 (4) ◽  
pp. 1356-1361 ◽  
Author(s):  
G F Tidmarsh ◽  
M O Dailey ◽  
I L Weissman

Mice genetically susceptible or genetically resistant to the leukemogenic effects of A-MuLV(Mo) were tested for their expression of the B-lineage neoplastic transformation-associated antigen, 6C3Ag. Genetically resistant inbred strains and recombinant inbred lines developed neither cells expressing high levels of 6C3Ag (6C3Aghi) in their hematolymphoid tissues nor Abelson leukemias. Genetically susceptible inbred strains and recombinant inbred lines developed high percentages of 6C3Aghi hematolymphoid cells concomitant with development of Abelson leukemias and lymphomas. Thus the genetically-determined resistance to A-MuLV(Mo) leukemogenesis appears to act at some step(s) after virus infection but before the stage of malignant progression, which is marked by 6C3Ag expression.


Genetics ◽  
1984 ◽  
Vol 107 (3) ◽  
pp. 447-461 ◽  
Author(s):  
Catherine Legraverend ◽  
Sirpa O Kärenlampi ◽  
Sanford W Bigelow ◽  
Peter A Lalley ◽  
Christine A Kozak ◽  
...  

ABSTRACT Aryl hydrocarbon (benzo[a]pyrene) hydroxylase inducibility by benzo[a]anthracene was studied in 29 somatic cell hybrid clones, developed by fusing mouse spleen or peritoneal cells from four different inbred strains with hypoxanthine phosphoribosyltransferase-deficient Chinese hamster E36 cells. Karyotype analysis plus 25 markers assigned to 16 autosomes and the X chromosome were examined. In 28 of the 29 clones, the presence or absence of inducibility is associated with the presence or absence, respectively, of mouse chromosome 17.—Liver microsomal aryl hydrocarbon hydroxylase induction by 3-methylcholanthrene or benzo[a]anthracene was assessed in appropriate backcrosses with the Mus musculus molossinus, M. m. castaneus, MOR/Cv, PL/J, SM/J and DBA/2J inbred strains and in 13 NX8 recombinant inbred lines. Twenty-seven biochemical genetic markers representing all but four autosomes were tested for possible linkage with the hydroxylase inducibility, and no linkage was found. The hepatic Ah receptor was quantitated in 26 BXD recombinant inbred lines; the Ah phenotype did not match exactly any of the more than 70 genes with established strain distribution patterns representing 12 autosomes and at least five unlinked markers.—It is concluded that a major gene controlling aryl hydrocarbon hydroxylase inducibility by benzo[a]anthracene is located on chromosome 17. Because there is no significant linkage with any of three biochemical markers in the upper third of the chromosome, we conclude that the inducibility gene is located in the distal 40% of mouse chromosome 17. Whether this trait represents the Ah locus, i.e., the gene encoding the cytosolic Ah receptor, will require further study.


Genetics ◽  
1986 ◽  
Vol 113 (3) ◽  
pp. 745-754
Author(s):  
Sharon L Liu ◽  
Robert P Erickson

ABSTRACT Hydrocortisone sodium phosphate was injected intramuscularly into A/J, C57BL/6J and recombinant inbred lines from these two parental lines to study the genetics of steroid-induced cleft palate in a situation of identical maternal and fetal genotypes. The strains were typed for H-2 (the major histocompatibility locus), β-glucuronidase and β2-microglobulin, which served as markers on chromosomes 17, 5 and 2, respectively. Hepatic glucocorticoid binding capacity had been previously measured in Hepes buffer and Hepes buffer plus dithiothreitol (DTT). The level of glucocorticoid binding in Hepes buffer and in Hepes plus DTT, as well as their ratio, was compared to the incidence of steroid-induced cleft palate in the recombinant inbred lines. A correlation was found between the response of glucocorticoid binding to DTT (expressed as a ratio of binding in the presence of DTT to binding without DTT) and hydrocortisone-induced cleft palate. When analyzing the effect of the three chromosomal markers on hydrocortisone-induced cleft palate, the b alleles of β2-microglobulin and of β-glucuronidase were associated with a higher incidence. Genetic analyses of the differences between these two inbred strains of mice in the incidence of steroid-induced cleft palate show it not to be monogenic.


2010 ◽  
Vol 67 (4) ◽  
pp. 435-440 ◽  
Author(s):  
Felipe André Sganzerla Graichen ◽  
José Antônio Martinelli ◽  
Luiz Carlos Federizzi ◽  
Marcelo Teixeira Pacheco ◽  
Márcia Soares Chaves ◽  
...  

Crown rust is the main disease affecting oats (Avena sativa L.), and genetic resistance has been the chief method utilized to control this disease. A population composed of 135 recombinant inbred lines, F5:6, generated by crossing the oat cultivar UFRGS 8 with the genotype Pc68/5*Starter, was assessed on the inheritance of resistance to crown rust (Puccinia coronata f. sp. avenae P. Syd. & Syd.). The evaluation of resistance in F5:6 seedlings was based on the type of infection resulting from inoculation with the race SQPT of P. coronata f. sp. avenae. The proportion of Resistant: Susceptible seedlings (R:S) was 62:64, which indicates that inheritance was governed by a single gene. The assessment of resistance inheritance in adult plants was performed in the field during the years 2004 and 2005. The distinction between resistant and susceptible classes was based on the final severity (FS) as well as the area under the disease progress curve, which was normalized and corrected (AUDPC*c). F5:6 and F5:7 were evaluated under field conditions in 2004 and 2005, demonstrating a ratio of approximately 1R:3S, which fits with a typical two genes inheritance model.


Genetics ◽  
1976 ◽  
Vol 83 (2) ◽  
pp. 373-377
Author(s):  
Benjamin A Taylor

ABSTRACT Four sets of recombinant inbred lines of mice have been used to analyze genetic differences in acute toxicity of the drug, isonicotinic acid hydrazide. Standard inbred strains, their F1 hybrids and recombinant inbred strains were all challenged with a single dose of the drug. The percent mortality of the different groups was analyzed to estimate heritability and the number of genes affecting resistance. The data indicated that resistance factors were dominant, heritability was moderate (.25-.37), and more than one gene was involved in each of four different sets of recombinant inbred lines. Possible approaches for identifying and mapping individual genes affecting resistance are discussed.


2019 ◽  
Vol 79 (01S) ◽  
Author(s):  
M. A. Saleem ◽  
G. K. Naidu ◽  
H. L. Nadaf ◽  
P. S. Tippannavar

Spodoptera litura an important insect pest of groundnut causes yield loss up to 71% in India. Though many effective chemicals are available to control Spodoptera, host plant resistance is the most desirable, economic and eco-friendly strategy. In the present study, groundnut mini core (184), recombinant inbred lines (318) and elite genotypes (44) were studied for their reaction to Spodoptera litura under hot spot location at Dharwad. Heritable component of variation existed for resistance to Spodoptera in groundnut mini core, recombinant inbred lines and elite genotypes indicating scope for selection of Spodoptera resistant genotypes. Only 29 (15%) genotypes belonging to hypogaea, fastigiata and hirsuta botanical varieties under mini core set, 15 transgressive segregants belonging to fastigiata botanical variety among 318 recombinant inbred lines and three genotypes belonging to hypogaea and fastigiata botanical varieties under elite genotypes showed resistance to Spodoptera litura with less than 10% leaf damage. Negative correlation existed between resistance to Spodoptera and days to 50 per cent flowering indicating late maturing nature of resistant genotypes. Eight resistant genotypes (ICG 862, ICG 928, ICG 76, ICG 2777, ICG 5016, ICG 12276, ICG 4412 and ICG 9905) under hypogaea botanical variety also had significantly higher pod yield. These diverse genotypes could serve as potential donors for incorporation of Spodoptera resistance in groundnut.


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