High impact information on PET18

• In this paper, we show that mutations in mak10 or the pet18 locus, which result in temperature-dependent replication of L-A dsRNA in vivo, also result in instability of the L-A dsRNA-containing (major class) viruslike particles in vitro [1].
• Crude host factor extracts prepared from mak3 or mak10ta mutants also support the reaction as effectively as that from a wild type strain, while a crude extract prepared from a pet18 mutant grown under the nonpermissive conditions is less effective [2].
• Two hit2 mutations, hit2-1 and hit2-2, were located on chromosome III and caused the deletion of the PET18 locus which has been shown to encode a gene required for growth at high temperatures [3].
• Xylose utilization was, however, not affected in strains in which YCR020C was overexpressed or deleted [4].
• However, despite their inability to maintain the killer RNA plasmid and mitochondrial DNA, pet18 mutants still can carry the other yeast plasmids, [URE3--1], [PSI], and 2-micron DNA [5].

Biological context of PET18

• We have isolated a yeast mutant, H53, with phenotypes identical to those of pet18 [6].

Other interactions of PET18

• (iii) [HOK] and [NEX] are both maintained in mak4, mak6, and mak27 strains (mak = maintenance of [KIL-k1]), but not in mak3, mak10, and pet18 strains [7].
• Dissecting the pet18 mutation in Saccharomyces cerevisiae: HTL1 encodes a 7-kDa polypeptide that interacts with components of the RSC complex [6].

References