# Binding of Transcriptional Activator to Silent Loci Causes Their Detachment from the Nuclear Lamina in Drosophila Neurons and Salivary Gland Cells

## TL;DR

This study shows that in Drosophila, transcriptional activators cause silent genes to move from the nuclear edge to the interior, similar to what happens in mammals.

## Contribution

The study demonstrates for the first time in Drosophila that transcriptional activator binding leads to chromatin repositioning from the nuclear lamina.

## Key findings

- Binding of GAL4 activator to silent loci in Drosophila causes detachment from the nuclear lamina.
- Relocalization of loci mimics gene activation in neurons.
- Results suggest conserved chromatin dynamics between mammals and Drosophila.

## Abstract

In mammals, the binding of transcriptional activators leads to the repositioning of silent loci from the nuclear periphery to the nuclear interior. However, it remained unknown whether the same mechanism functions in Drosophila. Here, using FISH and DamID, we have shown that binding the GAL4 activator to the silent loci causes weakening of their interactions with the nuclear lamina and relocalization inside nuclei in Drosophila salivary gland cells and neurons. This mimics the removal from the nuclear periphery of a neuron-specific gene upon its activation in neurons. Salivary gland cells contain polytene chromosomes with mechanical properties, different from chromosomes of diploid cells, while neurons represent predominantly non-dividing cell type. Our results indicate a causal relationship between transcriptional activator binding and changes in the intranuclear position of loci in Drosophila. They also point to the similarity in general chromatin dynamics in mammals and Drosophila, thus strengthening the role of model organisms in studying genome architecture.