The study demonstrates that differences in the expression levels of ev-2 and RAV-0 are not due to primary sequence differences in their long terminal repeats, suggesting modulation by other factors like methylation or cis-acting elements.
Rules out LTR sequence defects in ev-2 silencing; leaves open epigenetic or cis-acting modulation of retroviral expression.
A fragment of chicken DNA containing the left long terminal repeat of endogenous retrovirus ev-2 and flanking cellular sequences has been molecularly cloned and analyzed. Comparison with sequence data from the analogous regions of ev-1 and Rous-associated virus-0 viral DNA reveals similarities among flanking regions of the integrated proviruses and among all three long terminal repeats. From the latter finding, we conclude that the difference in level of expression of ev-2 and its progeny Rous-associated virus-0 provirus cannot be due to sequence differences in their upstream long terminal repeats.
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Scholl et al. (1983) studied this question.
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