The mammalian INO80 remodelling complex facilitates homologous recombination 
(HR), but the mechanism by which it does this is unclear. Budding yeast INO80 
can remove H2A.Z/H2B dimers from chromatin and replace them with H2A/H2B dimers. 
H2A.Z is actively incorporated at sites of damage in mammalian cells, raising 
the possibility that H2A.Z may need to be subsequently removed for resolution of 
repair. Here, we show that H2A.Z in human cells is indeed rapidly removed from 
chromatin flanking DNA damage by INO80. We also report that the histone 
chaperone ANP32E, which is implicated in removing H2AZ from chromatin, similarly 
promotes HR and appears to work on the same pathway as INO80 in these assays. 
Importantly, we demonstrate that the HR defect in cells depleted of INO80 or 
ANP32E can be rescued by H2A.Z co-depletion, suggesting that H2A.Z removal from 
chromatin is the primary function of INO80 and ANP32E in promoting homologous 
recombination.