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Yorkie ensures robust tissue growth in Drosophila ribosomal protein mutants.

Heterozygosity of a ribosomal protein gene causes a variety of developmental abnormalities in humans, which are collectively known as ribosomopathies, yet the underlying mechanisms remain elusive. Here, we analyzed Drosophila mutants heterozygous for a ribosomal protein gene, called Minute (M)/+ mutants. We found that, while M/+ flies develop essentially normal wings, simultaneous deletion of one copy of the Hippo pathway effector yki resulted in severe wing growth defects. These defects were caused by JNK-mediated cell death in the wing pouch via Eiger/TNF signaling. The JNK activation in M/+, yki/+ wing discs required a caspase Dronc, which is normally blocked by DIAP. Notably, heterozygosity of yki reduced DIAP1 expression in the wing pouch, leading to elevation of Dronc activity. Dronc and JNK formed a positive feedback loop that amplifies Dronc activation, leading to apoptosis. Our observations suggest a novel mechanism of robust tissue growth whereby tissues with reduced ribosomal protein prevent ectopic apoptosis via Yki activity.