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DKK2-MEDIATED SUPPRESSION OF WNT SIGNALING IS ESSENTIAL FOR ADULT HIPPOCAMPAL NEUROGENESIS AND COGNITIVE FUNCTION
Woo Seok Songand 4 co-authors
Seoul National University College of Medicine
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS01-07AM-235
Presentation
Date TBA
Board: PS01-07AM-235
Event Information
Poster Board
PS01-07AM-235
Poster
View posterAbstract
Dickkopf-related protein 2 (DKK2), a member of the DKK family (DKK1–4), modulates Wnt signaling, which plays a pivotal role in brain development and function. In contrast to other DKK family members, such as DKK1, DKK3, and DKK4, which are known negative regulators of Wnt signaling, the role of DKK2 in the brain remains poorly understood. Here, we demonstrate that DKK2-mediated suppression of Wnt signaling is essential for hippocampal function. Dkk2+/− mice exhibited impaired context discrimination accompanied by reduced adult hippocampal neurogenesis (AHN). Both genetic disruption of Dkk2 (Dkk2+/− and Dkk2−/−) and chronic intracerebral administration of DKK2 bidirectionally regulated AHN. Moreover, heterozygous and homozygous deletion of Dkk2 exerted distinct effects on hippocampal Wnt signaling. Complete loss of Dkk2 enhanced both canonical Wnt/β-catenin and noncanonical Wnt/planar cell polarity (PCP) signaling, whereas haploinsufficiency predominantly enhanced Wnt/PCP signaling. In hippocampal slices, DKK2 suppressed Wnt3a- and Wnt5a-induced activation of Wnt/β-catenin and Wnt/PCP signaling, respectively. Notably, chronic inhibition of c-Jun N-terminal kinase (JNK) signaling rescued the deficits in AHN and context discrimination observed in Dkk2+/− mice. Collectively, these findings identify DKK2 as a negative regulator of Wnt signaling that paradoxically promotes adult hippocampal neurogenesis and suggest that suppression of Wnt/PCP signaling may represent a potential strategy to enhance AHN.
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