Loss of the polarity protein Par3 promotes dendritic spine neoteny and enhances learning and memory

Voglewede, Mikayla M.; Ozsen, Elif Naz; Ivak, Noah; Bernabucci, Matteo; Tang, Ruizhe; Sun, Miao; Pang, Zhiping P.; Zhang, Huaye

doi:10.1016/j.isci.2024.110308

iScience

2024

DOI: 10.1016/j.isci.2024.110308

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Loss of the polarity protein Par3 promotes dendritic spine neoteny and enhances learning and memory

Mikayla M. Voglewede,

Elif Naz Ozsen,

Noah Ivak

et al.

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2024

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Neuronal connectivity, behavioral, and transcriptional alterations associated with the loss of MARK2

Caiola,

Wu,

et al. 2024

The FASEB Journal

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Neuronal connectivity is essential for adaptive brain responses and can be modulated by dendritic spine plasticity and the intrinsic excitability of individual neurons. Dysregulation of these processes can lead to aberrant neuronal activity, which has been associated with numerous neurological disorders including autism, epilepsy, and Alzheimer's disease. Nonetheless, the molecular mechanisms underlying abnormal neuronal connectivity remain unclear. We previously found that the serine/threonine kinase Microtubule Affinity Regulating Kinase 2 (MARK2), also known as Partitioning Defective 1b (Par1b), is important for the formation of dendritic spines in vitro. However, despite its genetic association with several neurological disorders, the in vivo impact of MARK2 on neuronal connectivity and cognitive functions remains unclear. Here, we demonstrate that the loss of MARK2 in vivo results in changes to dendritic spine morphology, which in turn leads to a decrease in excitatory synaptic transmission. Additionally, the loss of MARK2 produces substantial impairments in learning and memory, reduced anxiety, and defective social behavior. Notably, MARK2 deficiency results in heightened seizure susceptibility. Consistent with this observation, electrophysiological analysis of hippocampal slices indicates underlying neuronal hyperexcitability in MARK2‐deficient neurons. Finally, RNAseq analysis reveals transcriptional changes in genes regulating synaptic transmission and ion homeostasis. These results underscore the in vivo role of MARK2 in governing synaptic connectivity, neuronal excitability, and cognitive functions.

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Neuronal connectivity, behavioral, and transcriptional alterations associated with the loss of MARK2

Caiola,

Wu,

et al. 2024

The FASEB Journal

View full text Add to dashboard Cite

show abstract

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Loss of the polarity protein Par3 promotes dendritic spine neoteny and enhances learning and memory

Cited by 1 publication

References 107 publications

Neuronal connectivity, behavioral, and transcriptional alterations associated with the loss of MARK2

Neuronal connectivity, behavioral, and transcriptional alterations associated with the loss of MARK2

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