A new Mu induced mutation whose phenotype is suppressed in Mu-inactive tissue
--Michelle Nolasco and Alice Barkan

A Mu induced mutation, hcf106, was described previously, whose phenotype is modulated by the phase of Mu activity (Martienssen, R et al., EMBO J. 8:1633-1639,1989; Martienssen et al., Genes Dev. 4:331-343, 1990). Plants homozygous for hcf106 are pale green, non-photosynthetic, and seedling lethal when Mu is in its active phase. However, in Mu-inactive plants, the mutant phenotype is suppressed, i.e. leaves are dark green, and plants are viable. We have recently identified a new Mu-induced mutation whose phenotype responds in an analogous fashion to the phase of Mu activity.

psa1 arose in the Mu stocks propagated by the Hake and Freeling groups. Mutant seedlings are pale green with very small revertant sectors, and are non-viable due to the absence of the photosystem I complex. Rare plants in families segregating psa1 have large sectors of dark green tissue in young pale green leaves, with each successive leaf containing an increasing proportion of dark green tissue. This phenotype is very similar to that exhibited by hcf106 plants in which Mu became inactive during somatic development (Martienssen et al., 1990).

To test the possibility that suppression of the psa1 phenotype in dark green tissue was correlated with a change in Mu methylation status, DNA purified from pale green and dark-green sectors of two such plants was cut with HinfI and analyzed by Southern hybridization using a Mu1 probe. Dark green sectors from these plants contained primarily methylated Mu elements whereas pale green sectors from the same plants contained primarily unmethylated Mu elements. Fully mutant plants contained only unmethylated Mu elements. Therefore, the loss of the mutant phenotype in leaf tissue correlates with increased methylation of Mu elements.

Currently, we are testing this correlation between Mu methylation and suppression of the mutant phenotype by analyzing more sectored plants. To confirm that the mutant allele is retained in such plants, we will attempt to recover the mutant phenotype by crossing a viable Mu-inactive plant derived from a sectored seedling with a Mu-active plant heterozygous for psa1. In the future, the molecular mechanism will be elucidated that leads to suppression of the mutant phenotype in tissue containing methylated Mu elements. It will be interesting to compare this mechanism with that described previously for hcf106 (Barkan and Martienssen, Proc. Natl. Acad. Sci. USA 88:3502-3506, 1991). 

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