Interestingly, mutation of the three lysines to arginines reduced HD pathogenicity, as expression of unmodified Httex1p 97QP resulted in a rough eye phenotype in Drosophila, while expression of the K6R, K9R, K15R mutant gave almost no detectable phenotype, and resulted in decreased abundance of the Htt exon1 protein which may indicate that ubiquitination is not a requirement for degradation. Here, HTT is linked to Huntington disease.