Finally, we would like to thank all our co-authors, the lab members of the De Wit and Aerts lab, and especially our PIs @steinaerts.bsky.social and Joris De Wit for guidance and support throughout this project (8/n)

Finally, we use our prediction results to create a model of GRNs interactions surrounding Bcl6(+) and Smad3(+). Surprisingly, these predictions show sequential regulations, with early-active TFs delaying the activation of later GRNs and their putative synaptic targets (7/n)

Within the late-active GRNs, Smad3(+) is predicted to target several genes linked to synaptic organization and plasticity. We showed that loss of Smad3 in GCs alters inhibitory synaptic transmission without affecting the morphology of excitatory synaptic structures in these cells (6/n)

We tested the functional relevance of some of these GRNs in synaptic development of GCs. Within the middle-active GRNs, Bcl6(+) is predicted to target several synaptic genes. We found a novel role for Bcl6 regulating spine density and mossy fiber filopodia density in these cells (5/n)

Next, we created a RiboTag dataset of the granule cells. Interestingly, we found matching profiles between translatome and expression in the multiome dataset for most of GRNs of GCs (4/n)

To map the GRNs that control these synaptic gene changes, we created a multiome dataset of the hippocampus (P5-28). Our analysis using SCENIC+ identified 36 eRegulons with distinct activity patterns in mature GCs, which were separated in early-middle-late depending on their timing of activity (3/n)

We used SMART-Seq2 sequencing to detect a high number of genes in mature GCs, and found that synaptic genes show dynamic expression patterns, with early-postnatal genes related to cell morphogenesis and late-postnatal ones regulating synapse organization and plasticity (2/n)