Abstract
Condensin complexes are essential for mitotic chromosome assembly and segregation during cell divisions, however, little is known about their functions in post-mitotic cells. Here we report a role for the condensin I subunit Cap-G in Drosophila neurons. We show that, despite not requiring condensin for mitotic chromosome compaction, post-mitotic neurons express Cap-G. Knockdown of Cap-G specifically in neurons (from their birth onwards) results in developmental arrest, behavioural defects, and dramatic gene expression changes, including reduced expression of a subset of neuronal genes and aberrant expression of genes that are not normally expressed in the developing brain. Knockdown of Cap-G in mature neurons results in similar phenotypes but to a lesser degree. Furthermore, we see dynamic binding of Cap-G at distinct loci in progenitor cells and differentiated neurons. Therefore, Cap-G is essential for proper gene expression in neurons and plays an important role during the early stages of neuronal development.
Highlights
Differentiated neurons are post-mitotic cells – they lack the ability to further divide to produce daughter cells
Upon conducting a yeast-2-hybrid screen to look for proteins interacting with the neuron-specific transcription factor Lola-N, we were surprised to identify the condensin complex component Cap-G as a potential interacting partner
Whilst condensin activity has been characterised in neural stem cells (Nishide and Hirano, 2014), the role of condensin complexes in post-mitotic neurons has not yet been studied in any species
Summary
Differentiated neurons are post-mitotic cells – they lack the ability to further divide to produce daughter cells. Newly born neurons are not immediately ready to synapse with other neurons, nor generate action potentials. These immature cells undergo morphological changes, generating dendrites and axons, which will eventually form synapses with target cell(s) (Cajal, 1890). Underlying changes at the chromatin level are only just starting to be investigated. Chromatin accessibility and the 3D genome organisation all occur as neurons differentiate from progenitor cells (Yuen and Gerton, 2018; Hirano, 2016; Ganji et al, 2018; Kschonsak et al, 2017; Terakawa et al, 2017; Oliveira et al, 2005). Little is known about the mechanisms underlying this transition and the molecular factors that coordinate it
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