Isis Taylor

Depletion and replacement of tissue resident macrophages in mice with germ-line deletion of a conserved enhancer in the Csf1r locus.

This study shows that mice with a germ-line deletion of a Csf1r enhancer lack specific macrophages but maintain normal physiology and can be replenished by donor cells.

Homozygous kinase-dead Csf1r mutation in outbred mice reveals essential and redundant functions of tissue resident macrophages

This study shows that CSF1R-dependent macrophages are essential for hematopoiesis but many functions of tissue resident macrophages are redundant or strain-specific in mice.

A conserved distal element in the mouse Csf1r locus contributes to transcription in hematopoietic and trophoblast cells.

This study identifies a conserved regulatory element in the mouse Csf1r locus that contributes to transcription in hematopoietic and trophoblast cells, with partial redundancy with other enhancers.

Wild type bone marrow-derived microglia-like cells mitigate strain-dependent neuropathology in Csf1r mutant mice.

The paper shows that wild-type bone marrow-derived microglia-like cells reduce strain-dependent neuropathology in Csf1r mutant mice by preventing thalamic calcification.

The effect of a dominant kinase-dead Csf1r mutation associated with adult-onset leukoencephalopathy on brain development and neuropathology.

This study examines the impact of a heterozygous Csf1r mutation on brain development and neuropathology in mice, showing reduced microglial abundance and altered gene expression in disease models.

A kinase-dead Csf1r mutation associated with adult-onset leukoencephalopathy has a dominant-negative impact on CSF1R signaling.

This study investigates a kinase-dead Csf1r mutation in mice, showing it causes dominant-negative effects on CSF1R signaling and impacts macrophage development and brain microglia.