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Inhibition of precartilaginous chick somites by oncogenic virus
Abstract:
Infection of embryonic chicken notochord-somite explants with Rous sarcoma virus inhibited the in vitro differentiation of somites into cartilage. Visual inspection of the explants revealed that viral infection reduced the size of cartilage nodule formation. Formation of the complex of sulfated proteoglycans with hyaluronic acid was inhibited by RSV infection, and sedimentation analysis of the sulfated proteoglycans showed that very little fast sedimenting proteoglycans were synthesized by RSV-infected explants. The infected explants primarily synthesize a slowly sedimenting sulfated proteoglycan which was chondroitinase resistant. These slow-sedimenting sulfated proteoglycans lack the ability to associate with hyaluronic acid and appear to be noncartilaginous. These effects of RSV are apparently due to the src gene of this virus since the mutant td108, which lacks part of the src gene, has no detectable influence on the chondrogenic differentiation of somite explants. Similarly, infection with RAV-2 as well as with uv-irradiated virus had no detectable effect. The inhibition of synthesis of fast sedimenting proteoglycans was observed at 41 degrees C with explants infected with tsNY68, suggesting that residual activity of transforming gene of this virus at the non-permissive temperature is sufficient for this inhibition in the explants.
Insights
Rous sarcoma virus (RSV) infection hinders cartilage formation in chicken embryos by disrupting proteoglycan synthesis. The virus
Area of Science:
- Developmental Biology
- Virology
- Biochemistry
Background:
- Embryonic development involves complex cellular differentiation processes.
- Cartilage formation is a critical aspect of skeletal development.
- Viral infections can interfere with normal developmental pathways.
Purpose of the Study:
- To investigate the impact of Rous sarcoma virus (RSV) infection on in vitro chondrogenesis.
- To identify the specific viral mechanisms responsible for inhibiting cartilage differentiation.
- To analyze the effects of RSV on proteoglycan synthesis and structure.
Main Methods:
- Infection of embryonic chicken notochord-somite explants with Rous sarcoma virus (RSV).
- Visual assessment of cartilage nodule formation.
- Sedimentation analysis of sulfated proteoglycans synthesized by infected and control explants.
Main Results:
- RSV infection significantly reduced cartilage nodule size and formation.
- Viral infection inhibited the formation of sulfated proteoglycan complexes with hyaluronic acid.
- RSV-infected explants synthesized less fast-sedimenting proteoglycans and more chondroitinase-resistant, slow-sedimenting proteoglycans that do not associate with hyaluronic acid.
Conclusions:
- The src gene of Rous sarcoma virus is responsible for inhibiting chondrogenic differentiation.
- RSV disrupts normal proteoglycan synthesis, leading to the production of non-cartilaginous proteoglycans.
- The observed inhibition is linked to the viral src gene's activity, even at non-permissive temperatures for certain mutants.