This work would not have been possible without the dedicated, collaborative efforts of my colleagues, Madlaina Boillat and Marie Moulinier, from the @carleton-lab.bsky.social labs. 9/9

Finally, we demonstrate that NR4A2 is a master regulator of CLA and shell neuron identities, which, instead of directly activating or repressing their respective gene programs, recruits a transcription factor cascade involving NR2F2 and CUX1 in a dose-dependent manner. 8/9

We show that these phenotypes arise from an identity shift in CLA projection neurons, which reduce their expression of CLA marker genes and start expressing genes typical of shell projection neurons, a closely related cell type. 7/9

Alterations in gene expression and neuronal firing activity were accompanied by a marked reduction in CLA neuron abundance in Nr4a2 haploinsufficient mice. 6/9

Guided by the single-cell data, we provide a mechanistic explanation of the reduced excitability of CLA neurons in Nr4a2 haploinsufficient mice, which (briefly put) results from the recruitment of Ca2+-activated potassium channels. 5/9

Using an Nr4a2 haploinsufficiency model, we found that only claustrum (CLA) neurons exhibited significant transcriptomic alterations. 4/9

Employing a data-driven approach with smFISH labeling of coronal sections spanning four antero-posterior brain localizations, we constructed a versatile map of this brain area grounded in its cell types. 3/9

By combining single-cell RNA sequencing with MERFISH spatial transcriptomics, we characterized the transcriptomic identity and spatial organization of cell types and subtypes in the mouse claustro-insular region at high-resolution. 2/9