Biology subjects

Mui, K.

Publications and source records attributed to Mui, K..

2 recordsLinked to original sources

bioRxiv2025

The nucleus forms a dynamic contact with the plasma membrane to maintain the glandular epithelial architecture

The maintenance of epithelial architecture relies on precise mechanical and biochemical cues. Recent studies reveal an unexpected role for the nucleus in maintaining epithelial architecture, but how the nucleus is physically and molecularly integrated into epithelia remains unclear. Here, we identify a dynamic basal actin spot that links the nucleus to plasma membrane {beta}1-integrin through the linker of nucleoskeleton and cytoskeleton (LINC) in 3D breast acini. Depletion of LINC complex nesprin-2G, SUNs or FHOD1 disrupts nuclear positioning and inhibits lumen formation. Activation of a nesprin-2 degron causes acute loss of the basal actin spot and collapse of acini. Active Src and {beta}1-integrin accumulate in the basal actin spot and Src activity is required to prevent collapse of acinar structure. These findings reveal an unexpected mode of nuclear-plasma membrane contact that we propose homeostatically regulates intracellular contractility through a Src signaling pathway to maintain global epithelial architecture.

cell biology↗

bioRxiv2023

Sexual dimorphism in the social behaviour of Cntnap2 KO mice correlates with disrupted synaptic connectivity and increased microglial activity in the anterior cingulate cortex of males

A biological understanding of the apparent sex bias in autism is lacking. We have identified Cntnap2 KO mice as a model system to help better understand this dimorphism. Using this model, we observed social deficits in juvenile male KO mice only. These male-specific social deficits correlated with reduced spine densities of Layer 2/3 and Layer 5 pyramidal neurons in the Anterior Cingulate Cortex, a forebrain region prominently associated with the control of social behaviour. Furthermore, in male KO mice, microglia showed an increased activated morphology and phagocytosis of synaptic structures compared to WT mice, whereas no differences were seen in female KO and WT mice. Our data suggest that sexually dimorphic microglial activity may be involved in the aetiology of ASD, disrupting the development of neural circuits that control social behaviour by overpruning synapses at a developmentally critical period.

neuroscience↗