Tryptophan hydroxylase (TRH) loss of function mutations induce growth and behavioral defects in Daphnia magna.

ABSTRACT: Tryptophan hydroxylase (TRH) is the rate limiting enzyme in the serotonin synthesis. CRISPR-Cas9 technology was used to generate seven indel TRH mutants in Daphnia magna. Mono-allelic indel TRH-/+ clones showed normal levels of serotonin, measured by both immunohistochemistry and mass spectrometry (LC-MS/MS), whereas bi-allelic indel TRH-/- clones showed no detectable levels of serotonin. Life history and behavioral responses of TRH-/- clones showed the anti-phenotype of those exposed to selective serotonin reuptake inhibitors (SSRI). Mutants lacking serotonin grew less and hence reproduced latter, produced smaller clutches of smaller offspring and responded to a greater extent to light than wild type individuals. Mono-allelic indel TRH-/+ individuals showed the intermediate phenotype. The

SUBMITTER: Rivetti C 

PROVIDER: S-EPMC5784079 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature