Genome-wide analysis of 4 month old hippocampal gene expression in Neil3-deficent mice

ABSTRACT: Proliferative neural progenitor cells (NPCs) maintain high level of endogenous reactive oxygen species (ROS). Accumulation of ROS can cause oxidative DNA damage that may contribute to impaired neurogenesis. Adult neurogenesis is critical for hippocampus-dependent cognitive function. However, the functional consequences of oxidative base lesions on adult hippocampal neurogenesis remain largely unclear. Here, we found that DNA glycosylase Neil3 is required for the survival and physiological maturation of adult-born NPCs in the adult hippocampus. Impaired adult neurogenesis upon loss of Neil3 was correlated with reduced behavioral pattern separation. Interestingly this was not associated with decreased genomic integrity but with transcriptional regulation of GABAergic signaling. Our findings suggest that Neil3 acts as a positive regulator of adult hippocampal neurogenesis and is essential for normal pattern separation. Targeting Neil3 may have therapeutic potential for reversing age-related hippocampal dysfunction and cognitive decline. Overall design: The mRNA profiles from hippocampus of WT and Neil3-/- C57BL/6 mice at 4 month of age were generated by RNA sequencing using Illumina Hiseq 2000

INSTRUMENT(S): Illumina HiSeq 2000 (Mus musculus)

ORGANISM(S): Mus Musculus

SUBMITTER: Katja Scheffler 

PROVIDER: GSE118662 | GEO | 2019-06-01

REPOSITORIES: GEO