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. 2023 Jul 19;620(7973):366–373. doi: 10.1038/s41586-023-06357-1

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — a, UMAP projection of 10,375 inhibitory cortical neurons showing Sst44 enhancer accessibility. b, Accessibility of Sst subtype marker genes across Sst neurons. Max, maximum. c, AAV genome with the Sst44 enhancer driving NLS-mTagBFP2. ITR, inverted terminal repeat. d–f, The specificity of viral Sst44 expression was assessed using in situ RNA hybridization. d, The specificity of the Sst44 enhancer for Sst cells. e, The fraction of Sst44 cells that are positive for each subtype. f, The fraction of each Sst subtype that is Sst44-positive. Statistical analysis was performed using Wilcoxon rank-sum tests; **P < 0.01, *P < 0.05. g, The morphology of single Sst44 neurons filled through a whole-cell patch. Data are mean ± bootstrapped 95% confidence intervals.