Raw immunofluorescence images from "Knockout of Dectin-1 does not modify disease onset or progression in a MATR3 S85C knock-in mouse model of ALS"

Abstract: Microglia have been increasingly implicated in neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS). Dectin-1, encoded by the Clec7a gene, is highly upregulated in a specific microglial response state called disease-associated microglia (DAM) in various neurodegenerative conditions. However, the role of Dectin-1 in ALS is undetermined. Here, we show that Clec7a mRNA upregulation occurs in central nervous system (CNS) regions that exhibit neurodegeneration in a MATR3 S85C knock-in mouse model (Matr3^S85C/S85C) of ALS. Furthermore, a significant increase in the number of Dectin-1⁺ microglia coincides with the onset of motor deficits, and this number increases with disease progression. We demonstrate that the knockout of Dectin-1 does not affect survival, motor function, neurodegeneration, or microglial responses in Matr3^S85C/S85C mice. These findings suggest that Dectin-1 does not play a role in modifying ALS onset or progression.

Files: Details on the methods for immunofluorescence are described within the manuscript. Included in this dataset are all the raw immunostaining images used within the manuscript. The dataset is organized into folders that will provide details on which tissue is being imaged, the age of the mice, and the antibodies used. Note that the nomenclature used to indicate the genotype of double mutant mice (i.e., MATR3 S85C and CLEC7A KO) are WT or Hom (for homozygous). For example, for "MACL-M340 Hom Hom," MACL-M340 is the mouse ID, the first "Hom" means that the mouse was homozygous for the MATR3 S85C mutation, and the second "Hom" means that the mouse was homozygous for the CLEC7A KO.