No abstract

To fully exploit the potential of single-cell functional genomics in the study of development and disease, robust methods are needed to simplify the analysis of data across samples, time-points and individuals. Here we introduce a model-based factor analysis method, SDA, to analyze a novel 57,600 cell dataset from the testes of wild-type mice and mice with gonadal defects due to disruption of the genes Mlh3, Hormad1, Cul4a or Cnp. By jointly analyzing mutant and wild-type cells we decomposed our data into 46 components that identify novel meiotic gene-regulatory programs, mutant-specific pathological processes, and technical effects, and provide a framework for imputation. We identify, de novo, DNA sequence motifs associated with individual components that define temporally varying modes of gene expression control. Analysis of SDA components also led us to identify a rare population of macrophages within the seminiferous tubules of Mlh3-/- and Hormad1-/- mice, an area typically associated with immune privilege.

HighlightsInserting tPA leader sequence enhanced humoral responses of ChAdOx1 MERS.ChAdOx1 MERS elicited cellular immunity and neutralising antibodies.ChAdOx1 MERS responses were boosted by MVA MERS.Immunogenicity of a single dose of ChAdOx1 MERS was equivalent to 2 doses of MVA MERS.In MVA, F11 promoter enhanced cellular, but not humoral, immunogenicity, comparing to mH5 promoter.