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Expression of aldolase isozyme mRNAs in fetal rat liver

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The regulation of aldolase isozyme expression during development was studied by measuring the concentrations of mRNAs coding for aldolase A and B subunits in fetal and adult rat liver. Poly(A)‐containing RNAs were extracted from livers at various stages of development of fetal rats, and the aldolase A and B subunits in the in vitro translation products of these RNAs were analyzed immunologically. The content of aldolase B mRNA in 14‐day fetal liver, measured quantitatively as translational activity, was somewhat smaller than that of aldolase A mRNA; immunologically precipitable aldolase B and A amounted to 0.06% and 0.25%, respectively, of the total products. Similar experiments using RNAs from fetuses at later stages, however, showed that aldolase B mRNA increased during development, whereas aldolase A mRNA decreased. In newborn rat liver, aldolase B constituted 0.56% of the total translation products of mRNA, but there was little detectable aldolase A (0.03%).The changes of aldolase mRNA levels were analyzed further by northern blot and dot‐blot hybridization experiments using cloned aldolase A and B cDNAs. The content of aldolase B mRNA increased in the fetal stage, and that in newborn rat liver was about 12 times that in 14‐day fetal liver. In contrast, the aldolase A mRNA content decreased during gestation and that in newborn rat liver was about one‐eighth of that in 14‐day fetal liver. These observations suggest that the switch of aldolase isozyme expression in fetal liver is controlled by the levels of the respective mRNAs.
Title: Expression of aldolase isozyme mRNAs in fetal rat liver
Description:
The regulation of aldolase isozyme expression during development was studied by measuring the concentrations of mRNAs coding for aldolase A and B subunits in fetal and adult rat liver.
Poly(A)‐containing RNAs were extracted from livers at various stages of development of fetal rats, and the aldolase A and B subunits in the in vitro translation products of these RNAs were analyzed immunologically.
The content of aldolase B mRNA in 14‐day fetal liver, measured quantitatively as translational activity, was somewhat smaller than that of aldolase A mRNA; immunologically precipitable aldolase B and A amounted to 0.
06% and 0.
25%, respectively, of the total products.
Similar experiments using RNAs from fetuses at later stages, however, showed that aldolase B mRNA increased during development, whereas aldolase A mRNA decreased.
In newborn rat liver, aldolase B constituted 0.
56% of the total translation products of mRNA, but there was little detectable aldolase A (0.
03%).
The changes of aldolase mRNA levels were analyzed further by northern blot and dot‐blot hybridization experiments using cloned aldolase A and B cDNAs.
The content of aldolase B mRNA increased in the fetal stage, and that in newborn rat liver was about 12 times that in 14‐day fetal liver.
In contrast, the aldolase A mRNA content decreased during gestation and that in newborn rat liver was about one‐eighth of that in 14‐day fetal liver.
These observations suggest that the switch of aldolase isozyme expression in fetal liver is controlled by the levels of the respective mRNAs.

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