Null mutations were generated in the gene of by repeat-induced point mutation (RIP). The mutants were viable, lacked ergosterol, were resistant to the steroidal glycoside α-tomatine and were sensitive to the phytoalexins pisatin and biochanin A. RIP was frequently associated with silencing of the gene located adjacent to the duplicated sequence. The silencing of was reversible in the two cases examined and appeared to be due to the spread of cytosine methylation associated with RIP. The mutant could be complemented by transformation with recombinant genes that encode proteins chimeric for amino acid sequences from the transmembrane (TM) domain of human lamin B receptor (LBR). This indicates that the LBR TM domain possesses Δ-reductase activity.


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