Plants lacking WEE1 display normal development under control growth conditions, but are hypersensitive towards replication-inhibitory drugs. The underlying reasons for this hypersensitivity are currently unknown. Through the mapping of WEE1 complementation mutants we aim to uncover the mechanisms that account for the replication drug hypersensitivity of WEE1 deficient plants. In parallel, we aim to study WEE1 at the post-transcriptional level.