Spindle assembly checkpoint (SAC) ensures genome stability by delaying anaphase onset until all the chromosomes have achieved proper spindle attachment. Once correct attachment has been achieved, SAC must be silenced. In the absence of
mdf-1/MAD1, an essential SAC component, Caenorhabditis elegans cannot propagate beyond 3 generations. Previously, in a
dog-1(
gk10)/FANCJ mutator background, we isolated a suppressor of
mdf-1(
gk2) sterility (
such-4) which allowed indefinite propagation in the absence of MDF-1. We showed that
such-4 is a Cyclin B3 (
cyb-3) duplication. Here we analyze
mdf-1 such-4;
dog-1, which we propagated for 470 generations, with freezing of samples for long time storage at F170 and F270. Phenotypic analysis of this strain revealed additional suppression of sterility in the absence of MDF-1, beyond the effects of
such-4. We applied oligonucleotide array Comparative Genomic Hybridization (oaCGH) and whole genome sequencing (WGS) and identified a further amplification of
cyb-3 (triplication) and a new missense mutation in dynein heavy chain (
dhc-1). We show that
dhc-1(
dot168) suppresses the
mdf-1(
gk2), and is the second cloned suppressor, next to
cyb-3 duplication, that does not cause a delay in anaphase onset. We also show that amplification of
cyb-3 and
dhc-1(
dot168) cooperate to increase fitness in the absence of MDF-1.