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Genetic control of oncogenesis by murine sarcoma virus Moloney pseudotype. II. A dominant epistatic susceptibility
Abstract:
We have shown in the preceding paper that AKR mice are highly resistant to M-MSV tumor development, and that resistance is transmitted as a dominant character. In the present studies the tumor-response pattern of F1 hybrids between resistant AKR and susceptible strains (C57Bl/6, BALB/c and B10BR) following injection with Moloney mouse sarcoma virus (M-MSV) resembles that of the non-AKR parent. Segregation is observed in first backcross (Bc1) and F2 mice, and the segregation ratios up to Bc3 mice fit a one-gene model. The data of triple cross hybrids suggests that this dominant susceptibility gene inhibits the phenotypic expression of M-MSV tumor resistance in some susceptible Fv1bb strains as well as in their hybrids with AKR. Neither Fv-1 nor H-2 exerts any significant influence on this complex system.
Insights
AKR mice resist Moloney mouse sarcoma virus (M-MSV) tumors, a trait inherited dominantly. Susceptibility in hybrids suggests a single gene overrides resistance, independent of Fv-1 and H-2 loci.
Area of Science:
- Immunology
- Genetics
- Virology
Background:
- AKR mice exhibit high resistance to Moloney mouse sarcoma virus (M-MSV) induced tumors.
- This resistance is a genetically dominant trait.
- Understanding the genetic basis of M-MSV tumor development is crucial for cancer research.
Purpose of the Study:
- To investigate the genetic transmission of M-MSV tumor resistance and susceptibility.
- To identify the genetic factors influencing M-MSV tumor development in mice.
- To determine the role of specific genes (Fv-1, H-2) in this complex genetic system.
Main Methods:
- Cross-breeding experiments involving resistant AKR mice and susceptible strains (C57Bl/6, BALB/c, B10BR).
- Analysis of tumor response patterns in F1 hybrids, backcross (Bc1-Bc3), and F2 generations.
- Segregation analysis to fit genetic models.
Main Results:
- F1 hybrids between AKR and susceptible strains displayed tumor response patterns similar to the non-AKR parent.
- Segregation ratios in backcross and F2 generations supported a one-gene model for susceptibility.
- A dominant susceptibility gene appears to inhibit the phenotypic expression of M-MSV resistance.
Conclusions:
- A single gene controls dominant susceptibility to M-MSV tumor development.
- This susceptibility gene can override M-MSV resistance mechanisms.
- The Fv-1 and H-2 genetic loci do not significantly influence this M-MSV tumor response system.