Hjorth J J Johannes, Sterratt David C, Cutts Catherine S, Willshaw David J, Eglen Stephen J
Cambridge Computational Biology Institute, Department of Applied Mathematics and Theoretical Physics, University of Cambridge, Cambridge, CB3 0WA, United Kingdom.
Institute for Adaptive and Neural Computation, School of Informatics, University of Edinburgh, Edinburgh, EH8 9AB, United Kingdom.
Dev Neurobiol. 2015 Jun;75(6):641-66. doi: 10.1002/dneu.22241. Epub 2014 Nov 14.
Molecular and activity-based cues acting together are thought to guide retinal axons to their terminal sites in vertebrate optic tectum or superior colliculus (SC) to form an ordered map of connections. The details of mechanisms involved, and the degree to which they might interact, are still not well understood. We have developed a framework within which existing computational models can be assessed in an unbiased and quantitative manner against a set of experimental data curated from the mouse retinocollicular system. Our framework facilitates comparison between models, testing new models against known phenotypes and simulating new phenotypes in existing models. We have used this framework to assess four representative models that combine Eph/ephrin gradients and/or activity-based mechanisms and competition. Two of the models were updated from their original form to fit into our framework. The models were tested against five different phenotypes: wild type, Isl2-EphA3(ki/ki), Isl2-EphA3(ki/+), ephrin-A2,A3,A5 triple knock-out (TKO), and Math5(-/-) (Atoh7). Two models successfully reproduced the extent of the Math5(-/-) anteromedial projection, but only one of those could account for the collapse point in Isl2-EphA3(ki/+). The models needed a weak anteroposterior gradient in the SC to reproduce the residual order in the ephrin-A2,A3,A5 TKO phenotype, suggesting either an incomplete knock-out or the presence of another guidance molecule. Our article demonstrates the importance of testing retinotopic models against as full a range of phenotypes as possible, and we have made available MATLAB software, we wrote to facilitate this process.
分子线索和基于活性的线索共同作用,被认为可引导脊椎动物视网膜轴突到达其在视顶盖或上丘(SC)的终末位点,以形成有序的连接图谱。其中涉及的机制细节以及它们相互作用的程度仍未完全清楚。我们开发了一个框架,在此框架内,可以根据从小鼠视网膜-上丘系统整理的一组实验数据,以无偏且定量的方式评估现有的计算模型。我们的框架便于模型之间的比较,根据已知表型测试新模型,并在现有模型中模拟新表型。我们使用这个框架评估了四个代表性模型,这些模型结合了Eph/ephrin梯度和/或基于活性的机制以及竞争机制。其中两个模型从其原始形式进行了更新,以适应我们的框架。这些模型针对五种不同的表型进行了测试:野生型、Isl2-EphA3(ki/ki)、Isl2-EphA3(ki/+)、ephrin-A2,A3,A5三敲除(TKO)和Math5(-/-)(Atoh7)。两个模型成功再现了Math5(-/-)前内侧投射的范围,但其中只有一个能够解释Isl2-EphA3(ki/+)中的塌陷点。这些模型需要在SC中存在一个较弱的前后梯度,以再现ephrin-A2,A3,A5 TKO表型中的残余秩序,这表明要么是敲除不完全,要么存在另一种导向分子。我们的文章证明了针对尽可能全面的表型测试视网膜拓扑模型的重要性,并且我们提供了我们编写的MATLAB软件以促进这一过程。