The DNA structure checkpoint protein Rad26 ATRIP  is also required for an interphase microtubule damage response. This checkpoint delays spindle pole body separation and entry into mitosis following treatment of cells with microtubule poisons. This checkpoint requires cytoplasmic Rad26 ATRIP , which is compromised by the  rad26:4A  allele that inhibits cytoplasmic accumulation of Rad26 ATRIP  following microtubule damage. The  rad26::4a  allele also disrupts minichromosome stability and cellular morphology, suggesting that the interphase microtubule damage checkpoint pathway operates in an effort to maintain chromosome stability and proper cell shape. To identify other proteins of the Rad26-dependent interphase microtubule damage response, we used ultra violet (UV) radiation to identify extragenic interaction suppressors of the  rad26::4A  growth defect on microtubule poisons. One suppressor mutation, which we named  mut2a , permitted growth of  rad26:4A  cells on MBC media and conferred sensitivity to a microtubulin poison upon genetic outcross. In an attempt to clone this interaction suppressor using a genomic library complementation strategy, we instead isolated  pap1   +  as an extracopy suppressor of the  mut2a  growth defect. We discuss the mechanism by which  pap1   +  overexpression may allow growth of  mut2a  cells in conditions that destabilize microtubules.