The polyadenylation inhibitor cordycepin (3 ' dA) causes a decline in c-MYC mRNA levels without affecting c-MYC protein levels

Study of the distribution of the poly(A) tail length of c-myc mRNA in sever al cell lines revealed a distinct, prevailing population with short poly(A) tails, derived through sequential deadenylation, To elucidate the possible in vivo function of this distinct short failed c-myc mRNA population, the polyadenylation inhibitor cordycepin was used, This resulted in a decline i n steady state c-myc mRNA levels with the remaining messenger mostly oligoa denylated, However, c-MYC proteins did not follow the reduction of the c-my c mRNA, On the other hand, in cells exposed to physiological agents known t o downregulate c-myc expression, the reduction of mRNA steady state levels, was reflected upon c-MYC protein levels, The dissociation between c-myc mR NA and protein levels caused by cordycepin was not dare to the stabilizatio n of the c-MYC proteins and was not an indiscriminate effect since in the p resence of cordycepin, c-fos mRNA and protein levels concomitantly declined , Our data indicate that under these conditions, a long poly(A) tail is not instrumental for c-myc mRNA translation and furthermore, the discrepancy i n the steady state of c-myc mRNA level: c-MYC protein ratio between control cells and cells treated with cordycepin indicates that c-myc mRNA is subje cted to translational control.