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<p>Genetically modified rabies virus can map neural circuits retrogradely from genetically determined cells. However, similar tools for anterograde tracing are not available. Here, we describe a method for anterograde transsynaptic tracing from genetically determined neurons based on a rationally designed protein, ATLAS. Expression of ATLAS in neurons causes presynaptic release of a payload composed of an antibody-like protein, AMPA.FingR, which binds to the N terminus of GluA1, and a recombinase. In the synaptic cleft, AMPA.FingR binds to GluA1, causing the payload to be endocytosed into postsynaptic cells and delivered to the nucleus, where it triggers expression of a recombinase-dependent reporter. In mice, ATLAS mediates monosynaptic transneuronal tracing from random or genetically determined cells that is strictly anterograde, synaptic and nontoxic. Moreover, ATLAS-mediated tracing shows activity dependence, suggesting that it can label active circuits underlying specific behaviors. Finally, ATLAS is composed of modular components that can be independently replaced or modified.</p>

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ATLAS: a rationally designed anterograde transsynaptic tracer

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年5月1日

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  • Jacqueline F. Rivera,
  • Haoyang Huang,
  • Weiguang Weng,
  • Heesung Sohn,
  • Allison E. Girasole,
  • Shun Li,
  • Madeline A. Albanese,
  • Melissa Qin,
  • Can Tao,
  • Molly E. Klug,
  • Sadhna Rao,
  • Ronald Paletzki,
  • Bruce E. Herring,
  • Scott E. Kanoski,
  • Li I. Zhang,
  • Charles R. Gerfen,
  • Bernardo L. Sabatini,
  • Don B. Arnold

摘要

Genetically modified rabies virus can map neural circuits retrogradely from genetically determined cells. However, similar tools for anterograde tracing are not available. Here, we describe a method for anterograde transsynaptic tracing from genetically determined neurons based on a rationally designed protein, ATLAS. Expression of ATLAS in neurons causes presynaptic release of a payload composed of an antibody-like protein, AMPA.FingR, which binds to the N terminus of GluA1, and a recombinase. In the synaptic cleft, AMPA.FingR binds to GluA1, causing the payload to be endocytosed into postsynaptic cells and delivered to the nucleus, where it triggers expression of a recombinase-dependent reporter. In mice, ATLAS mediates monosynaptic transneuronal tracing from random or genetically determined cells that is strictly anterograde, synaptic and nontoxic. Moreover, ATLAS-mediated tracing shows activity dependence, suggesting that it can label active circuits underlying specific behaviors. Finally, ATLAS is composed of modular components that can be independently replaced or modified.