Molecular and genetics inquiry program using Drosophila eyes absent gene.

The aim of this study was to develop molecular genetics inquiry programs using the eyes absent gene of Drosophila melanogaster. The program was composed of various molecular genetics experiments, including mutation observation, cross-breeding, searching for genetic information in web databases, gDNA extraction, and PCR. Each experiment was designed to include a reasoning process, thus aligning the program closely with the structure of authentic scientific research. This program was also developed with a modular design to provide flexibility in its implementation. The program was implemented for middle school students affiliated with a university science education institute for the gifted, and surveys indicated that students had positive experiences with the program. Our findings suggest that the program provides students with a contextual understanding of how authentic research is conducted. Finally, we suggest ways to implement the program effectively.

Phosphatidylserine synthase plays an essential role in glia and affects development, as well as the maintenance of neuronal function.

Phosphatidylserine (PS) is an integral component of eukaryotic cell membranes and organelles. The Drosophila genome contains a single PS synthase (PSS)-encoding gene (Pss) homologous to mammalian PSSs. Flies with Pss loss-of-function alleles show a reduced life span, increased bang sensitivity, locomotor defects, and vacuolated brain, which are the signs associated with neurodegeneration. We observed defective mitochondria in mutant adult brain, as well as elevated production of reactive oxygen species, and an increase in autophagy and apoptotic cell death. Intriguingly, glial-specific knockdown or overexpression of Pss alters synaptogenesis and axonal growth in the larval stage, causes developmental arrest in pupal stages, and neurodegeneration in adults. This is not observed with pan-neuronal up- or down-regulation. These findings suggest that precisely regulated expression of Pss in glia is essential for the development and maintenance of brain function. We propose a mechanism that underlies these neurodegenerative phenotypes triggered by defective PS metabolism.