scholarly journals A new allele of the lpr locus, lprcg, that complements the gld gene in induction of lymphadenopathy in the mouse.

1990 ◽  
Vol 171 (2) ◽  
pp. 519-531 ◽  
Author(s):  
A Matsuzawa ◽  
T Moriyama ◽  
T Kaneko ◽  
M Tanaka ◽  
M Kimura ◽  
...  
Keyword(s):  
Recessive Gene ◽  
Mutant Gene ◽  
Inbred Strains ◽  
Lymphoid Hyperplasia ◽  
Lymphoid Cells ◽  
Autoantibody Production ◽  
Genetic Studies ◽  
Inbred Strains Of Mice ◽  
Backcross Populations ◽  
Generalized Lymphadenopathy

Several mice with generalized lymphadenopathy were found in the CBA/KlJms (CBA) colony maintained at our institute. A new mutant strain of mice that develop massive lymphoid hyperplasia at 100% incidence within 5 mo after birth was established by crossing these diseased mice. Genetic studies on lymphadenopathy were conducted in F1, F2, and backcross populations from crosses between mutant CBA (CBA-m) and various inbred strains of mice. The results supported the control of lymphadenopathy by a single autosomal recessive gene. Since C3H/He-gld/gld (C3H-gld), MRL/MpJ-lpr/lpr (MRL-lpr), and C3H/HeJ-lpr/lpr (C3H-lpr) mice develop the same type of lymphoid hyperplasia, allelism of the mutant gene with gld or lpr was tested by investigating lymphadenopathy in F1 and backcross populations from crosses between CBA-m and C3H-gld, MRL-lpr, or C3H-lpr mice. The gene was confirmed to be allelic with lpr but not with gld. Interestingly, however, the mutant gene interacted with gld to induce less severe lymphadenopathy. Thus, the mutant gene was named lprcg, an lpr gene complementing gld in induction of lymphoproliferation. The genetic conclusion was supported by the same profile of surface markers of lymphoid cells with gld/gld, lpr/lpr, lprcg/lprcg, lprcg/lpr, and +/gld +/lprcg genotypes, as well as by massive lymph node hyperplasia and high titers of autoantibodies in the first four genotypes, but slight hyperplasia and insignificant autoantibody production in the last. The discovery of lprcg provided strong genetic evidence for the parallels between anomalous phenotypes of gld and lpr, and CBA/KlJms-lprcg/lprcg mice will contribute to elucidation of the mechanism of induction of the same abnormal differentiation and functions of lymphocytes by gld and lpr.

scholarly journals The immune response of allophenic mice to the synthetic polymer L-glutamic acid, L-lysine, L-phenylalanine. II. Lack of gene complementation in two nonresponder strains

1977 ◽  
Vol 145 (3) ◽  
pp. 766-771 ◽  
Author(s):  
CM Warner ◽  
JL McIvor ◽  
PH Maurer ◽  
CF Merryman
Keyword(s):  
Immune Response ◽  
Glutamic Acid ◽  
Relative Proportion ◽  
Cell Types ◽  
Inbred Strains ◽  
Parental Cell ◽  
Lymphoid Cells ◽  
Gene Complementation ◽  
Inbred Strains Of Mice ◽  
Normal Environment

The genetic control of the immune response of inbred strains of mice to certain antigens has been demonstrated to be governed by a set of Ir genes linked to the major histocompatibility complex (H-2) of mice (1,2). Until recently, the control was thought to be governed by single, dominant genes, located within the I region of the H-2 complex. Merryman et al. (3) originally demonstrated that the immune response to the synthetic terpolymer L-glutamic acid, L-lysine, L-phenylaline (GLφ) is under dominant, H-2-linked Ir gene control (4-7). This was shown both by crossing two nonresponder parental strains to produce responder offspring in the F(1) generation, and by the analysis of appropriate recombinant stains of mice. The two complementing genes have been mapped in the IA and IC regions of the H-2 complex, and have been termed β and α, respectively (5,6). Thus, any strain of mouse may contain neither, one, or both genes. Only mice containing both genes are capable of responding to GLφ. It has been shown using F(1) hybrid and recombinant strains of mice, that the α- and β-genes can complement each other in either the cis (on the same chromosome) or in the trans (on different chromosomes) position (8). In this paper we report the results of studies aimed at answering the question of whether or not the α- and β- genes can complement each other when they are present in different lymphoid cells. To this end we have constructed allophenic mice composed of two nonresponder strains (A and C57BL/6), which show gene complementation in the F(1) generation. Allophenic mice are chimeras containing two cell types coexisting in a normal environment. The mice were tested for the specific cellular composition of the two parental cell types and were found to possess a complete range in the relative proportion of the two cell types. This report demonstrates that regardless of the mixture of cell types present in the allophenic mice, none of them were responders to GLφ. Thus no complementation of the α- and β-genes is seen when the two genes are present in different cells.

scholarly journals Strongyloides venezuelensis infection susceptibility of seven inbred strains of mice

2002 ◽  
Vol 54 (3) ◽  
pp. 273-278 ◽  
Author(s):  
A.F.T. Amarante ◽  
T.C.G. Oliveira-Sequeira
Keyword(s):  
Primary Infection ◽  
Inbred Mice ◽  
Inbred Strains ◽  
Genetic Studies ◽  
Infective Larvae ◽  
Inbred Strains Of Mice ◽  
Strongyloides Venezuelensis ◽  
Infection Susceptibility ◽  
The Mean ◽  
Small Intestines

A trial was carried out to investigate the susceptibility of seven strains of mice to Strongyloides venezuelensis primary and secondary experimental infections, in order to provide the basis for genetic studies about resistance. Twelve six-week-old male inbred mice of the A/J, BALB/c, CBA/J, C3H/Hepos, C57BL/6, DBA/2 and NIH strains were infected s.c. with 2000 infective larvae. The mean worm counts (± SD) in the small intestine six days after infection were, in increasing order: 28 (± 19) in NIH; 647 (± 228) in BALB/c; 709 (± 425) in DBA/2; 731 (± 151) in C3H/Hepos, 801 (± 174) in CBA/J; 1024 (± 267) in C57BL/6 and 1313 (± 483) in A/J. C57BL/6 mice showed the highest fecal egg counts and NIH, the lowest. No eggs in fecal exams or nematodes in small intestines were recovered from animals reinfected 14 days after primary infection. NIH strain was highly resistant to primary infection by S. venezuelensis. The most susceptible of the other six strains appeared to be the C57BL/6 strain which presented a high nematode counting in intestine and the highest egg output.

Autosomal recessive inheritance of airway hyperreactivity to 5-hydroxytryptamine

1989 ◽  
Vol 67 (3) ◽  
pp. 1125-1132 ◽  
Author(s):  
R. C. Levitt ◽  
W. Mitzner
Keyword(s):  
Airway Hyperresponsiveness ◽  
Autosomal Recessive ◽  
Present Report ◽  
Recessive Gene ◽  
Autosomal Recessive Inheritance ◽  
Inbred Strains ◽  
Airway Hyperreactivity ◽  
Recessive Trait ◽  
Inbred Strains Of Mice ◽  
Airway Response

We have previously reported that airway hyperresponsiveness to acetylcholine (ACh) is inherited as an autosomal recessive trait in A/J and C3H/HeJ mice and the progeny of crosses between them (FASEB J. 2: 2605–2608, 1988). In the present report, we have extended these studies by evaluating the biological variability in the airway response to 5-hydroxytryptamine (5-HT) and ACh among multiple genetically standardized inbred strains of mice. The pattern of airway responsiveness to ACh differed significantly from that of 5-HT in nine inbred strains of mice. A/J mice showed nonspecific airway hyperresponsiveness to both 5-HT and ACh. DBA/2J mice were hyperresponsive to 5-HT but not to ACh. An airway phenotype that resembled these inbred strains is termed HYPERREACTIVE. The C3H/HeJ and C57BL/6J inbred strains were minimally reactive to either ACh or 5-HT. Airway phenotypes that resembled these minimally reactive strains are termed HYPOREACTIVE. The frequency of HYPERRACTIVE and HYPOREACTIVE offspring from crosses between A/J and C3H/HeJ mice or DBA/2J and C57BL/6J mice is consistent with a single autosomal recessive gene, primarily determining airway hyperresponsiveness to 5-HT. We report linkage studies which suggest that these genes are not closely linked and that 5-HT and ACh airway hyperresponsiveness is inherited independently. The results of these studies suggest that murine nonspecific airway hyperresponsiveness is determined by multiple genes.

Susceptibility to ozone-induced inflammation. II. Separate loci control responses to acute and subacute exposures

1993 ◽  
Vol 264 (1) ◽  
pp. L21-L26 ◽  
Author(s):  
S. R. Kleeberger ◽  
R. C. Levitt ◽  
L. Y. Zhang
Keyword(s):  
Airway Inflammation ◽  
Polymorphonuclear Leukocytes ◽  
Inflammatory Responses ◽  
Single Gene ◽  
Inbred Strains ◽  
Acute Exposure ◽  
Genetic Studies ◽  
Strain Distribution Pattern ◽  
Inbred Strains Of Mice ◽  
Subacute Exposure

We demonstrated previously that inbred strains of mice are differentially susceptible to acute (3 h) and subacute (48 h) exposures to 2 parts per million (ppm) ozone (O3) and 0.30 ppm O3, respectively. Genetic studies with O3-resistant C3H/HeJ and O3-susceptible C57BL/6J strains have indicated that susceptibility to each of these O3 exposures is under Mendelian (single gene) control. In the present study, we hypothesized that the same gene controls susceptibility to the airway inflammatory responses to 2 ppm and 0.30 ppm O3 exposures. To test this hypothesis, airway inflammation was induced in 10 BXH and 16 BXD recombinant inbred (RI) strains of mice by acute as well as subacute O3 exposures. Airway inflammation was assessed by counting the number of polymorphonuclear leukocytes (PMNs) in bronchoalveolar lavage (BAL) returns obtained immediately after 48-h subacute exposure to 0.30 ppm O3, or 6 h after 3 h acute exposure to 2 ppm O3. Each RI strain was classified as susceptible or resistant to each exposure, based on a comparison of mean numbers of PMNs with those of the respective progenitor strains. For each RI set, a phenotypic strain distribution pattern (SDP) was thus derived for each exposure regimen, and the SDPs were then compared for concordance. Among the BXH RI strains, 4 of 10 responded discordantly to the two exposures: 3 were susceptible to acute exposure and resistant to subacute exposure, whereas 1 was conversely susceptible. Among the BXD RI strains, 4 of 16 were discordant: 1 was susceptible to acute exposure, and resistant to subacute exposure, whereas 3 were conversely susceptible.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of Foster Nursing on Alcohol Selection in Inbred Strains of Mice

1972 ◽  
Vol 33 (2) ◽  
pp. 494-503 ◽  
Author(s):  
Setsuo Komura ◽  
Masao Ueda ◽  
Toshikiyo Kobayashi
Keyword(s):  
Inbred Strains ◽  
Inbred Strains Of Mice
Sign in / Sign up

Export Citation Format

Share Document