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Background  Genetic alterations in human topoisomerase II alpha ( TOP2A ) are linked to cancer susceptibility. TOP2A decatenates chromosomes and thus is necessary for multiple aspects of cell division including DNA replication, chromosome condensation and segregation. Topoisomerase II alpha is also required for embryonic development in mammals, as mouse  Top2a  knockouts result in embryonic lethality as early as the 4-8 cell stage. The purpose of this study was to determine whether the extended developmental capability of zebrafish  top2a  mutants arises from maternal expression of  top2a  or compensation from its  top2b  paralogue.    Results  Here, we describe  bloody minded (blm) , a novel mutant of zebrafish  top2a . In contrast to mouse  Top2a  nulls, zebrafish  top2a  mutants survive to larval stages (4-5 day post fertilization). Developmental analyses demonstrate abundant expression of maternal  top2a  but not  top2b . Inhibition or poisoning of maternal topoisomerase II delays embryonic development by extending the cell cycle M-phase. Zygotic  top2a  and  top2b  are co-expressed in the zebrafish CNS, but endogenous or ectopic  top2b  RNA appear unable to prevent the  blm  phenotype.    Conclusions  We conclude that maternal  top2a  enables zebrafish development before the mid-zygotic transition (MZT) and that zebrafish  top2a  and  top2b  are not functionally redundant during development after activation of the zygotic genome.

Maternal topoisomerase II alpha, not topoisomerase II beta, enables embryonic development of zebrafish top2a -/- mutants