Ribosomal protein mutation suppresses gonadal leader cell migration defects inmig-17/ADAMTSmutants inCaenorhabditis elegans

Abstract

AbstractThe migration of the gonadal distal tip cells (DTCs) inCaenorhabditis elegansprovides an excellent model for studying the migration of epithelial tubes during organogenesis. Mutations in themig-17/ADAMTSgene cause misdirected migration of DTCs during gonad formation, resulting in deformed gonad arms. An amino-acid substitution in RPL- 20 corresponding to the mammalian RPL18a/eL20, a component of the 60S ribosomal large subunit, showed a slow growth phenotype and strongly suppressed themig-17gonadal defects. Slow-growing mutantsclk-1andclk-2also suppressedmig-17, although weaker thanrlp-20mutants. MIG-17 recruits FBL-1C/fibulin-1C to the gonadal basement membrane to regulate DTC migration. Reducing the gene dosage offbl-1by half partially compromised the suppressor activity of the mutantrpl-20gene onmig-17. Analysis using the mNeonGreen-FBL-1 reporter revealed that its localization to the gonadal basement membrane was significantly reduced inmig-17, whereas it was recovered to the wild-type levels inmig-17; rpl-20double mutants. These results indicate that therpl-20mutation suppressesmig-17gonadal defects through dual mechanisms: deceleration of growth rate and enhancement of FBL-1C recruitment to the gonadal basement membrane.