Nup107 is a crucial regulator of Torso-mediated metamorphic transition in Drosophila melanogaster

The holometabolous metamorphosis in Drosophila is governed by neuropeptide hormone signaling, culminating in the surge of 20-hydroxyecdysone levels and ecdysone receptor signaling. Nucleoporins (Nups) form nuclear pore complexes, influencing nucleocytoplasmic transport, cell division, and gene regulation. The Nup107-160 complex (Y-complex) members have been studied in disease and organism development, and we have explored the role of Nup107 in Drosophila development.

Here, we report a unique regulation exerted by the Nup107 in metamorphic transition during Drosophila development. Nup107 depletion induces developmental arrest in third-instar larvae, impeding tissue growth and a complete cessation of pupariation. This lack of pupariation is due to the loss of EcR nuclear translocation and inhibited downstream transcriptional activation. We argue that Nup107 modulates the EcR activation pathway by controlling the ecdysone biosynthesis, as Nup107 depletion negatively impacts the transcription of the Halloween genes. Feeding ecdysone to Nup107 -depleted larvae restores normal EcR signaling and metamorphosis. Overexpression of the receptor tyrosine kinase, torso , and MAP-kinase pathway activator, ras, in Nup107 depletion background rescued the developmental delay phenotypes. Through our observations, we propose that Nup107 is a key regulator of Torso-mediated activation of EcR signaling required for the ecdysone at larval to pupal metamorphic transition in Drosophila .