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Published on: October 13, 2014
CONTROL OF SYNTHESIS OF RNA AND PROTEIN IN DIAPAUSING AND INJURED CECROPIA PUPAE
Insights
Injury to cecropia silkworm moth pupae stimulates RNA and blood protein synthesis. Actinomycin D at low doses selectively inhibits new protein synthesis, suggesting differential messenger RNA regulation.
Area of Science:
- Developmental biology
- Molecular biology
- Insect physiology
Background:
- Injury to diapausing cecropia silkworm moth pupae triggers physiological responses.
- These responses include increased RNA and blood protein synthesis.
- A specific 'injury protein' is precociously synthesized upon injury.
Purpose of the Study:
- To investigate the role of RNA synthesis in injury-induced protein production.
- To determine the effect of Actinomycin D on specific protein synthesis pathways.
- To elucidate the regulatory mechanisms of gene expression in response to injury.
Main Methods:
- Inducing injury in diapausing cecropia silkworm moth pupae.
- Administering Actinomycin D at different concentrations (2 µg/g and 0.5 µg/g).
- Analyzing RNA and de novo blood protein synthesis, including 'injury protein'.
Main Results:
- Injury stimulates RNA and blood protein synthesis in all pupal tissues.
- Actinomycin D (2 µg/g) blocks both increased blood protein synthesis and 'injury protein' synthesis.
- Actinomycin D (0.5 µg/g) inhibits 'injury protein' synthesis but not other blood protein synthesis.
Conclusions:
- Low concentrations of Actinomycin D selectively inhibit the synthesis of new messenger RNAs.
- Existing messenger RNAs in production can continue synthesis at lower Actinomycin D concentrations.
- This suggests differential regulation of gene expression for specific proteins during injury response.
Abstract:
Injury to diapausing pupae of the cecropia silkworm moth stimulates the synthesis of RNA in all pupal tissues and the synthesis of several blood proteins; such injury also induces the precocious synthesis of a protein, termed "injury protein," which normally appears in the blood during adult development. Actinomycin D, injected in concentrations of 2 micrograms per gram of body weight, blocks the injury-stimulated increase in blood protein synthesis and the injury-induced synthesis of injury protein. However, at concentrations of 0.5 micrograms per gram it prevents the induction of injury-protein synthesis but does not prevent the increased synthesis of other blood proteins. These results suggest that low concentrations of actinomycin may inhibit the synthesis of new kinds of messenger RNA but still permit the continued synthesis of messenger RNA's already in production at the time the actinomycin is injected.
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