Interrelationship between the Bcg and Tbc-1 genes

The relationship of the mouse Bcg and Tbc-1 genes was studied. It was shown that the F1 hybrids between highly susceptible to tuberculosis mice I/St (Tbc-1s) and the Bcgs-carrying strains were highly resistant to M. tuberculosis H37Rv infection. These results point to complementation of Bcgs and Tbc-1s genes. Analysis of survival time of the [(AKR x B10-fzy)F1 x B10-Fzy]BC1 offspring showed that the mouse chromosome 1 does not regulate resistance to H37Rv infection. No linkage of the Tbc-1s gene with chromosome 1 was revealed when using fzy gene as a marker of the chromosome 1.     

A new erythrocytic antigen of C57BL/10 (B10) mice

A new antigen, detectable on murine erythrocytes by hemagglutination assay with a (BALB/cCrl X SWR/J)F1 anti-B10.D2n/Sn alloantiserum, is described. Among the inbred and congenic mouse strains tested for reactivity with the antiserum, only the immunizing strain, B10.D2, and its congenic resistant partner, C57BL/10 (B10), reacted. Three other C57 strains, C57BL/6J, C57BL/6By, and C57L, were negative for the antigen. F1 hybrids between B10 and BALB/c, an antigen-negative strain, were positive for the antigen indicating that its expression is dominant. Typing of 39 (BALB/c X (BALB/c X B10)F1) and 62 [BALB/c X B10)F1 X BALB/c) backcross mice revealed that a single gene controls expression of the antigen. The gene is autosomal and not linked to H-2, Ly-4, or the c (albino) or b coat color genes.     

Genetic control of the content and avidity of antigen-binding B-lymphocytes in the mouse spleen]

The content (per 10 nucleated cells) and avidity curves of IgM positive B-lymphocytes forming rosettes with trinitrophenyl-sheep erythrocytes (TNP-RFC) were compared in two mouse lines (BALB/c C57BL/6), F1 hybrids (BALB /c X C57BL/6) and backcross hybrids (F1 X BALB/c, F1 X C57BL/6). Trinitrophenyl-bovine serum albumin (TNP24BSA) and dinitrophenyl-bonvine serum albumin (DNP23BSA) and sulfanil-BSA (Sulf17-BSA) in different dilutions were used as inhibitors. BALB/c spleen contained by 60% more TNP-RFC than C576/6 spleen. F1 hybrids (F1 X BALB/c) contained on the average by 35% more TNP-RFC than (F1 X C57BL/6). Inhibition curves (avidity curves) were essentially different in the two mouse lines and F1 hybrids. A conclusion was drawn that the TNP-REC content and avidity were under a strong genetic control. Together with the assumption of random expression of V-genes (idiotype genes?) in the lymphocytes the above data suggest that the simplest mechanism of the genetic control could be a definitive ratio between the corresponding groups of V-genes.     

An X-encoded alloantigenicity between BALB/c and C57BL/6 strains of mice

To detect minor barriers to histocompatibility that might be encoded on the X chromosome in mice, we grafted reciprocal sets of (C57BL/6xBALB/c)F1, (C57BL/6xDBA/2)F1, and (BALB/cxDBA/2)F1 mice with tail skin from the respective paternal inbred strain. Our histogenic analysis suggests that, compared with the C57BL/6 mouse strain, the BALB/c strain generates X-linked antigen loss. In contrast, we detected no X-linked histogenic differences between strains C57BL/6 and DBA/2, or DBA/2 and BALB/c. To localize this X-linked barrier to histocompatibility, we produced a panel of 25 [(BALB/cxC57BL/6)F1xC57BL/6]N2 males that were grafted with C57BL/6 skin to determine which carried the BALB/c-derived component(s) necessary for graft rejection. DNA marker analysis showed one region of overlapping BALB/c-derived X-chromosomal segments among the graft rejecters, suggesting that this antigen-loss haplotype ( H-hix(c), for histoincompatibility on the X chromosome, c haplotype) may be restricted within the DXMit55 to the Xq telomere interval (which excludes only the centromeric tip of the X). Further backcrossing of H-hix(c) to C57BL/6 resulted in fewer rejecter mice than expected by the N4 generation, suggesting that a second, unlinked locus is also involved in this X-linked alloantigenicity. The vigorous rejection of male (C57BL/6xBALB)F1 and female (B6.C- H2(d)xC57BL/6)F1 skin by (BALB/cxC57BL/6)F1 males, as well as the assessment of markers on Chromosome 17 among N2 and N4 graft-recipient males, suggests that this second locus is H2, and that H-hix(b)-encoded alloantigens require both H2(b) and H2(d)-encoded presentation molecules for efficient graft rejection.     

Sex and H-2 haplotype control the resistance of CBA-BALB hybrids to the induction of T cell lymphoma by Moloney leukemia virus

CBA/N and CBA/CaHN have a significantly longer latent period than other inbred mouse strains between infection with Moloney murine leukemia virus and the appearance of T cell lymphoma. The genetic characteristics of this resistance have been analyzed in the F1 hybrids of CBA/N and CBA/CaHN with BALB H-2 congenic strains. Sexual phenotype and H-2 haplotype significantly influenced survival in the F1 hybrids of CBA/CaHN with BALB. In the F1 with BALB/cJ and BALB/cAnN (both H-2d), the males survived significantly longer than the females; but in the F1 with BALB.K (H-2k) and BALB.B (H-2b), the survival of males and females was the same. Survival was not prolonged by the recessive X-linked immunodeficiency gene xid or other genes on the CBA/N X-chromosome, because the (CBA/N X BALB/c)F1 male and the reciprocal (BALB/c X CBA/N)F1 male, which does not carry the CBA X-chromosome, were equally resistant. H-2 haplotype did not influence survival among the BALB H-2 congenics, and sex had little effect on the resistance of the CBA and BALB parents. These results demonstrate that a sex-dependent gene linked to H-2 significantly influences the expression of CBA genes for lymphoma resistance in the F1 hybrid with BALB.     

Immune response to the H-X antigen on P815-X2

In a preceding report, the detection of an H-2-linked immune response to the H-X ^d antigen on the P815-X2 mastocytoma was demonstrated by the significantly increased survival of (C57BL/6 × DBA/2)F₁ (B6D2F1) male hybrids (H-X ^b ) compared with female siblings (H-X ^{b/H-X d} ) after injection with the histocompatible tumor (H-X ^d ). This interpretation was supported by the absence of this sex effect in reciprocal D2B6F1 hybrids (H-X ^d and H-X ^{d/H-X b} ). Additional findings presented in this paper support the conclusion that this sex effect is due to a true immunological response to H-X ^d : (a) Reciprocal (DBA/2 × C57BL/6 H-2 mutant)F₁ hybrids, as well as D2B6F1, failed to exhibit the sex effect: (b) the demonstration of the sex effect in (BALB/c × DBA/2)F₁ and (BALB/c-H-2 ^dm2 × DBA/2)F₁ hybrids and in (C57BL/10 × DBA/2)F₁ hybrids was consistent with the known H-X incompatibilities between the strains BALB/c and DBA/2 and C57BL/10 and DBA/2, respectively, previously demonstrated by skin grafting; and (c) the sex effect was not abrogated by castration of male B6D2F1 hybrids. Variability in the presence or absence of the sex effect was observed in various [recombinant inbred (RI) × DBA/2]F₁ hybrids and may be attributed to the influence of a regulatory non-H-2 gene which is closely linked to the gene coding for mouse kidney-androgen-regulated protein (KAP) but androgen-independent, or to variability in inheritance of the H-X ^b allele among the RI lines. It is proposed that the P815-X2 model may be utilized to type RI lines derived from a cross between C57BL/6 and DBA/2 for their H-X genotypes.Abbreviations B C57BL/6 origin allele - B6 C57BL/6 - B10 C57BL/10 - B6D2F1 (C57BL/6 × DBA/2)F₁ - B6 ^m D2F1 (C57BL/6 H-2 mutant × DBA/2)F₁ - bm10 B6.C-H-2 ^bm10 - C BALB/c - D DBA/2 origin allele - D2 DBA/2 - dm2 BALB/c-H-2 ^dm2 - H-X X chromosome-determined histocompatibility antigen of the mouse - Ir gene, immune response gene - KAP kidney androgenregulated protein - MST median survival time - RI recombinant inbred - SDP strain distribution pattern     

Genetic interactions in induction of endogenous murine leukemia virus from low leukemic mice

The frequency of ecotropic murine leukemia virus (MuLV) production in cells induced with halogenated pyrimidines has been investigated in several low leukemic strains of mice. Very few BALB/c or C57BL/6 (B6) induced embryo cells produce MuLV; this low frequency increases 10 to 50 fold in cells of the BALB/c × B6 F1 hybrid. Data from back-crosses of the F1 hybrid to each parent and from BALB/c × B6 recombinant inbred strains indicate that the phenotype of enhanced MuLV production results from interaction of two unlinked loci, dominant (+/+) alleles of which are carried by either parent. Genetic tests with BALB/c × B6 recombinant inbred strains confirm this two-locus model. The loci are designated Inc-1 and Inb-1 to signify their phenotypic detection by induction and the BALB/c or B6 strain of origin, respectively. Examination of hybrids of BALB/c and of B6 with other strains indicates that strains related in pedigree to BALB/c carry Inc-1, whereas those related to B6 carry Inb-1. Identification of genetic loci that specifically interact to enhance MuLV production after exposure to halogenated pyrimidines indicates the existence of mechanisms that regulate the induction or intracellular expression of endogenous MuLV.     

Comparison of patterns of hybrid resistance to the BALB/c plasmacytomas LPC-1 and MPC-11

Summary Patterns of genetic control of hybrid resistance to the BALB/c plasmacytoma LPC-1 were studied for comparison with those to MPC-11, a plasmacytoma investigated previously. The overall patterns of hybrid resistance to the two tumors were similar, i.e., hybrids between BALB/c and BALB congenic resistant (CR) strains, A and A CR strains, SJL and DBA/2 were as susceptible to LPC-1 as BALB/c mice themselves, whereas hybrids between BALB/c and AKR, C57BL/Ks, DBA/1, C57BL/6 (B6), C57BL/10 (B10) and B10 CR strains were resistant to LPC-1 as previously shown with MPC-11. Heterozygosity within the H-2 complex alone was insufficient for resistance to either tumor. Among hybrids between BALB/c and the B10 CR strains, however, the presence of certain H-2 haplotypes influenced the degree of resistance seen and this H-2 effect was different for the two tumors. A sex effect on resistance to LPC-1, but not to MPC-11, was seen among F₁ hybrids between BALB/c and DBA/1 although not in any other F₁ hybrids. Among ((B10×BALB/c)F₁×BALB/c) and (BALB/c×(B10×BALB/c)F₁) and ((BALB/c×B10)F₁×BALB/c) and ((BALB/c×B10)F₁×BALB/c) backcross mice, however, significantly more males than females were resistant to LPC-1 and the results of this study are compatible with the idea that in F₁ hybrids between BALB/c and B10, resistance to LPC-1 is controlled by two dominant autosomal genes, one of which is sex-limited and neither of which is linked to H-2. In contrast, hybrid resistance to MPC-11 in this cross is controlled by a single gene. Cross-protection experiments indicated that the two tumors share at least one tumor-associated transplantation antigen.     

Strain difference in mouse natural killer activity augmented by mouse interferon and poly I.C

The level of natural killer (NK) activity was found to vary considerably among several mouse strains. In vivo and in vitro, interferon (IFN) and IFN inducers have been shown to augment mouse NK activity. C3H/He mice showed high NK activity, DDD/1 and A/J mice low NK activity, and C57BL/6, BALB/c and DBA/2 mice intermediate NK activity after injection with polyinosinic polycytidylic acid (poly I. C.). The same NK activity correlation was observed in nontreated mice, but the NK activities were lower compared with the poly I. C.-injected mice. Moreover, the DDD/1 and A/J mice showed almost no augmentation of NK activity on injection with poly I.C. In vivo, C3H/He, BALB/c and C57BL/6 mice injected with IFN showed augmented NK activity, but DDD/1 mice showed no such reaction. In vitro, C3H/He, BALB/c and C57BL/6 mouse spleen cells treated with IFN also showed augmented NK activity, but DDD/1 mouse spleen cells showed almost none. F1 hybrids between high (C3H/He) and low (DDD/1) NK-activity strains showed high NK activity. Thus, activity is dominant over low activity. The segregation of (DDD/1 X C3H/He) Fl X DDD/1 back-cross mice suggested that the strain differences in NK activity are under polygenic control.     

T cell clone-specific alloantisera that inhibit or stimulate antigen-induced T cell activation

Pigeon cytochrome c-specific, IL 2-secreting T cell hybrids have been used for immunizations to generate alloantibodies against the T cell antigen receptor on these cells. The B10.A-derived cloned T cell hybrid 2B4 was emulsified in complete Freund's adjuvant and injected i.p. into several F1 strains of mice. After boosting the recipient animals with cells in incomplete Freund's adjuvant, malignant ascites developed. In the (BALB/c X AKR)F1 or (AKR X BALB/c)F1 strains, these ascites consistently contained material that specifically inhibited the antigen-induced IL 2 secretion of only the immunizing 2B4 cell. The inhibitory material was antibody that specifically bound and could be absorbed only by 2B4. A similar immunization was performed with the cell 2C2. Although this cell apparently has similar antigenic fine specificity as 2B4, high concentrations of ascites generated by 2C2 immune animals inhibited antigen-induced IL 2 release only from 2C2. At lower concentrations of ascites, this preparation synergized with antigen to increase the IL 2 release, again only from 2C2. This antibody preparation did not affect concanavalin A-induced IL 2 release. The most likely explanation for these data is that the ascites contain antibodies that react with the antigen-specific receptor on the T cell hybrids.     

Dimethylnitrosamine metabolism: II. In vitro activation of dimethylnitrosamine by hepatic and renal tissues from crosses among BALB/c, DBA and C57BL mice

Crosses among BALB/c, C57BL and DBA mice were performed to investigate the genetic mechanisms involved in metabolism of DMN by renal and hepatic tissues. Liver S-9 fractions from parental strain DBA had the greatest potential to activate DMN and liver fractions from parental strain BALB/c had the lowest. No age or sex-related differences were observed within strain. Crossing of either C57BL or DBA to BALB/c mice resulted in F1 hybrids with liver microsomal enzymes that gave results similar to the BALB/c parental strain. There were no sex or age differences within crossbred strains in the potential of liver to activate DMN. In contrast male DBA and C57BL parental mice renal S-9 fractions did not differ significantly from each other but did differ significantly from male BALB/c renal fractions and from female and immature animals of all strains. Crossing of either DBA or C57BL mice with BALB/c mice resulted in male F1 hybrids whose renal S-9 fractions did not differ significantly from males of the parental BALB/c strain. In all instances, male renal S-9 fractions had a significantly greater potential to activate DMN than female or immature animals. F1 DBA X C57BL hybrids had renal S-9 fractions that did not differ significantly from the parental strains. These data suggest that the gene(s) for low DMN metabolism of BALB/c mice are apparently dominant over the genes from both DBA and C57BL. The exact genetic or physiological mechanism needs further elucidation.     

Genetic Analysis of Nucleotide Triphosphatase Activity in the Mouse Brain

A Ca(2+)- or Mg(2+)-stimulated ecto-ATPase is thought to regulate the hydrolysis of extracellular ATP in nervous tissues. The hydrolysis of nucleotide triphosphates (NTPs) was analyzed in brain microsomal fractions from crosses of DBA/2J (D2) and C57BL/6J (B6) mice. The nucleotide triphosphatase (NTPase) activity was significantly reduced in D2 mice as compared to B6 mice, and B6D2F(1) hybrids had activities intermediate to the parentals. A significant positive correlation was found between the hydrolysis of four NTPs (ATP, CTP, GTP and UTP) in 24 B6 X D2 (BXD) recombinant inbred (RI) strains of mice and in 80 B6D2F(1) X D2 backcross mice. The RI strains and backcross mice fell into two distinct groups with respect to the NTPase activity. Linkage of NTPase activity was suggested with the chromosome 2 markers, D2Mit6 and Ass-1, in the RI strains, and was confirmed by analysis of other markers in the backcross population. These data suggest that the Ca(2+)- or Mg(2+)-stimulated hydrolysis of NTPs, designated Ntp, is regulated by a single gene located on proximal chromosome 2. Although an association was observed previously between Ca(2+)-ATPase activity and susceptibility to audiogenic seizures (AGS), no significant association was observed for the expression of Ntp and AGS susceptibility.     

MuMTV antigen expression and mammary tumor incidence in non-inbred dd mice

The expression of mammary tumor virus (MTV) antigen in the milk and various organs of three non-inbred dd mouse stocks (ddO, ddN and ddY) was examined by the immunodiffusion (ID) and micro-immunodiffusion (micro-ID) tests. The rate of MTV antigen expression in the milk was 100% at the first lactation in ddO (6/6) and ddN mice (10/10), and 23% in ddY mice (3/13). Mammary tumor incidence was 13% (mean tumor age: 12.0 months), 32% (9.6 months) and 10% (11.5 months) in ddO, ddN and ddY mice, respectively, In F1 hybrids between MTV-free BALB/c females and dd males, a high level of MTV antigen was detected by the ID test in the milk of (BALB/c X ddO) F1, however, the levels in (BALB/c X ddN) F1 and (BALB/c X ddY) F1 mice were low at the first lactation and elevated with the advance of lactation number. Mammary tumor incidence had a trend to be higher and earlier in these F1 hybrids than in non-inbred dd stocks. The development of mammary tumors and detection of MTV antigen in F1 hybrids indicate the extrachromosomal transmission of MTV by male dd mice. The micro-ID test has shown that the mammary tumors, mammary glands, male genital organs except for the testis and the salivary gland expressed MTV antigen, with a high frequency of suggesting that secondary male genital organs may play an important role in MTV infection in mice.     

Interleukin-2 production during murine infection by Leishmania mexicana amazonensis

Highly susceptible BALB/c mice, resistant C57B1/6 and their F1 progeny (BDF1) were infected subcutaneously in the foot pad with Leishmania mexicana amazonensis. At various times after infection, spleen or draining popliteal lymph node cells were assayed for their capacity to generate Interleukin-2 (I1-2) by Concanavalin A (ConA) stimulation. In both BALB/c and C57B1/6 strains there was a transient increase in their capacity to produce I1-2, from the 3rd to the 10th week post-infection. Return to pre-infection levels occurred between 13th to 16th week post-infection in all three strains. BALB/c mice always produced higher titers of I1-2 than C57B1/6, but such differences were statistically significant only at 3 and 10 weeks post-infection. BDF1 mice had titers similar to those observed in BALB/c mice. I1-2 production by ConA-stimulated lymph node cells was lower as compared to the spleen, but with a similar pattern among the three mice strains. Our data show that susceptibility to infection by L. mexicana amazonensis is not associated with deficient ConA-stimulated I1-2 production.     

Neonatal tolerance induction in the thymus to MHC-class II-associated antigens. II. Significance of MHC antigens in anti-Mls tolerance

Specificity of anti-Mlsa tolerance induced in BALB/c (H-2d, Mlsb) neonates was investigated by a popliteal lymph node (PLN)-swelling assay for the local graft-versus-host (GVH) reaction by injecting tolerant thymus cells into the footpads of several types of F1 hybrid mice. When thymus cells were obtained from 1-week-old normal BALB/c, they evoked enlargement of PLNs of (BALB/c X DBA/2)F1 (H-2d, Mlsb/a) [CDF1] recipients and of other hybrid recipients, heterozygous in Mlsa,c,d alleles, irrespective of the major histocompatibility complex (MHC) haplotypes. The same thymus cells did not cause the response in MHC-heterozygous F1 hybrids when the hybrids were homozygous in Mlsb, identical with BALB/c mice. Therefore, the PLN response to Mls antigens, known to be closely associated with MHC-class II antigens, was not directed to the class II antigens themselves. This enabled us to examine the effects of MHC on tolerance induction to the Mls antigens. When BALB/c neonates were injected with CDF1 bone marrow cells, complete tolerance to Mlsa-H-2d antigens of CDF1 cells was induced in the thymus, while responsiveness to Mlsa antigens in the context of H-2k and H-2b antigens, was not affected. This indicates MHC-restriction of neonatal tolerance to Mls antigens. Furthermore, when Mls and H-2-heterozygous (BALB/c X AKR)F1 (H-2d/k, Mlsb/a) bone marrow cells served as the tolerogen, thymus cells of BALB/c neonates were also tolerized to Mlsa-H-2k antigens as well as to Mlsa-H-2d antigens, which suggests the involvement of MHC, probably class II antigens of tolerance-inducing cells.     

Tests of genetic allelism between four inbred mouse strains with absent corpus callosum.

Inbred mouse strains that lack the corpus callosum connecting the cerebral hemispheres in the adult differ from the C57BL/6J strain at several relevant but unknown loci. To identify at least one major locus that influences axon guidance, different strains showing phenotypically similar defects were crossed to test for allelism. If the F1 hybrid between two strains with the same brain defect is phenotypically normal, it is much more likely that the two strains will differ at fewer loci than will an acallosal strain and C57BL/6J. This approach proved to be very informative. Five reasonable models of inheritance involving two or three loci were assessed, and the data justified rejection of all but one hypothesis. A total of 479 mice were obtained from four inbred strains prone to absence of the corpus callosum (BALB/cWah1, BALB/cWah2, I/LnJ, and 129/ReJ), one normal strain (C57BL/6J), and 11 F1 hybrids among them. Because the size of forebrain axon bundles is generally greater in mice with larger brains, and because whole brain size is certainly polygenic, the phenotypically normal groups were used to derive a standard index of the degree of corpus callosum deficiency relative to brain size. Results demonstrated clearly that the hybrid between BALB/cWah1 and 129/ReJ is normal, whereas the crosses among the BALB/c substrains and I/LnJ yielded many mice with deficient corpus callosum. I/LnJ crossed with 129/ReJ also produced some animals with callosal defects. The data were consistent with a model in which the difference between BALB/c and 129/ReJ involves two loci, whereas the defect in I/LnJ involves homozygosity at three loci, which impairs development more severely.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparative analysis of T lymphocytes recovered from the lungs of mice genetically susceptible, resistant, and hyperresistant to Mycobacterium tuberculosis-triggered disease

Genetic control of susceptibility to tuberculosis (TB) is being intensively studied, and immune responses to mycobacteria are considerably well characterized. However, it remains largely unknown which parameters of response distinguish resistant and susceptible TB phenotypes. Mice of I/St and A/Sn inbred strains and (A/Sn x I/St)F(1) hybrids were previously categorized as, respectively, susceptible, resistant, and hyperresistant to Mycobacterium tuberculosis-triggered disease. In the present work we compared parameters of lung T cell activation and response following M. tuberculosis challenge. In all mice, the disease progression was accompanied by a marked accumulation in the lungs of activated CD4(+) (CD44(high)/CD45RB(low)) and CD8(+) (CD44(high)/CD45RB(+)) T cells capable of secreting IFN-gamma and of activating macrophages for NO production and mycobacterial growth inhibition. However, significantly more CD8(+) T cells were accumulated in the lungs of resistant A/Sn and F(1) compared with I/St mice. About 80% A/Sn and F(1) CD8(+) cells expressed CD44(high)/CD45RB(+) phenotype, while about 40% I/St CD8(+) cells did not express CD45RB marker at week 5 of infection. In contrast, in susceptible I/St mice lung CD4(+) cells proliferated much more strongly in response to mycobacterial sonicate, and a higher proportion of these cells expressed CD95 and underwent apoptosis compared with A/Sn cells. Unseparated lung cells and T cells of I/St origin produced more IL-5 and IL-10, respectively, whereas their A/Sn and F1 counterparts produced more IFN-gamma following infection. F(1) cells overall expressed an intermediate phenotype between the two parental strains. Such a more balanced type of immune reactivity could be linked to a better TB defense.     

Fertility in intersubspecific hybrids of laboratory mice (Mus musculus domesticus) and molossinus mice (M. m. molossinus)

We studied the reproductive performance of F1 and F2 hybrids of laboratory mice (C57BL/6, B6 and BALB/c) and molossinus mice (MOM and Mol-A). The F1 x F1 crosses were fully fertile. In the F2 x F2 crosses, the copulation rate was slightly lower and the pregnancy rate was markedly depressed: only 5 out of 18 copulated females (27.8%) became pregnant in the F2 hybrids derived from the reciprocal crosses of B6 x MOM, and in the F2 hybrids from BALB/c x Mol-A crosses, the pregnancy rate was 51.4% (18/35). This low fertility was attributed mainly to the F2 females, because there was a much lower pregnancy rate (56.5%; 26/46) in the (B6 x MOM)F2 female x B6 male crosses compared with the B6 female x (B6 x MOM)F2 male crosses (80.6%; 26/32). On the other hand, the pregnant F2 females were judged to have normal reproductive ability, based on observations of the numbers of corpora lutea, implantations and live fetuses at day 14 of pregnancy. Apparently there is segregation of fertile and sterile females at the F2 generation, but it remains to be determined how the loss of fertility is brought about in the sterile F2 females.     

Genetic control of juvenile growth rate in mice: variation between a congenic strain and its background strain

Studies on the genetic regulation of growth are confounded by the multigenic basis of growth. There is a need to isolate simplified genetic systems for the study of growth. We compared two closely related mouse strains and their F1 hybrids with regard to birth and weaning weights. The strains we used were C57BL/6 (B6) and a congenic derivative of B6 (HW54) that contains a short segment of BALB/c chromosome 7 spanning the H-24 and Gpi-1 loci. Despite the genetic similarity of these strains, they differed significantly in both birth and weaning weights. At birth, B6 pups were on average as much as 6.6% heavier than were pups from HW54. By the time of weaning, this trend was reversed; HW54 pups were as much as 13.8% heavier than were B6 pups. (B6 x HW54)F1 hybrids were intermediate between the parental strains in birth weight but were identical to B6 animals at weaning. An analysis of the F2 generation suggested that postnatal growth differences between B6 and HW54 are probably dependent on the maternal genotype. These strain-specific growth rates result from polymorphism at a restricted portion of the genome and represent a highly simplified system for the study of the genetics of growth.