Indiana University

Transposons and paramutation

--Drew Schwartz

Paramutation, as defined by Brink, is a directed heritable change in one allele induced by the presence of a second allele in a heterozygote. According to this definition, the reactivations of inactive, methylated forms of transposable elements induced by the introduction of an active element into the genome, such as has been described for Spm, Mu and Ac, also represent cases of paramutation. Homologous transposable elements must be considered alleles even if they have been transposed to other sites in the genome. This communication is concerned with the direction of the paramutational change. Whereas, in the case of non-jumping genes, such as R and B, the change is from the active to the inactive condition, the direction is the reverse for the transposable elements, from inactive to the active state. I suggest that all the cases of paramutation involve the same basic mechanism; that R and B paramutations also involve transposable elements and the direction of the change depends upon whether one scores the state of the element or the state of the gene locus in which the element resides. This hypothesis is based on the principle that the presence of a transposable element in a gene locus can suppress the function of the gene when the element is in the active state, but that the same gene can be functional when the element is in the methylated, inactive condition. The inverse relationship between the functioning of the Wx gene and the methylation state of the Ac element in the wx-m7 allele is a prime example (McClintock, Carnegie Inst. Wash. Year Book 64:527-536, 1965; Chomet et al. EMBO J. 6:295-302, 1987). The hypothesis will be developed for paramutation at the B locus but the same scheme could apply for R. I propose that there is a methylated, inactive form of a transposon-like element in the B locus. The transposon is also defective in that although it has the potential to make transposase it itself cannot transpose, possibly as a result of a mutation in one of the termini. In the paramutated B' allele, the element is in the non-methylated, active form, causing a shut-down in the functioning of the B gene. Activation of the methylated transposon in the B allele, induced by the transposase produced by the active element in B, would cause the B -> B' paramutational change observed in B/B heterozygotes. This requires 100% activation of the inactive transposon and a report of such a high level of reactivation for Ac is in press. In the case of R, the presence of a transposon in the paramutagenic R-st allele is indicated by its variegated phenotype.

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