Showing 1 - 3 of 3 results
1.
Optogenetic inhibition of light-captured alcohol-taking striatal engrams facilitates extinction and suppresses reinstatement.
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Vierkant, V
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Xie, X
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Huang, Z
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He, L
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Bancroft, E
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Wang, X
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Nguyen, T
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Srinivasan, R
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Zhou, Y
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Wang, J
Abstract:
Alcohol use disorder (AUD) is a complex condition, and it remains unclear which specific neuronal substrates mediate alcohol-seeking and -taking behaviors. Engram cells and their related ensembles, which encode learning and memory, may play a role in this process. We aimed to assess the precise neural substrates underlying alcohol-seeking and -taking behaviors and determine how they may affect one another.
2.
Optogenetic inhibition of light-captured alcohol-taking striatal engrams facilitates extinction and suppresses reinstatement.
Abstract:
Alcohol use disorder (AUD) is a complex condition, and it remains unclear which specific neuronal substrates mediate alcohol-seeking and -taking behaviors. Engram cells and their related ensembles, which encode learning and memory, may play a role in this process. We aimed to assess the precise neural substrates underlying alcohol-seeking and -taking behaviors and determine how they may affect one another.
3.
WNK kinases sense molecular crowding and rescue cell volume via phase separation.
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Boyd-Shiwarski, CR
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Shiwarski, DJ
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Griffiths, SE
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Beacham, RT
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Norrell, L
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Morrison, DE
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Wang, J
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Mann, J
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Tennant, W
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Anderson, EN
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Franks, J
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Calderon, M
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Connolly, KA
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Cheema, MU
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Weaver, CJ
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Nkashama, LJ
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Weckerly, CC
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Querry, KE
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Pandey, UB
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Donnelly, CJ
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Sun, D
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Rodan, AR
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Subramanya, AR
Abstract:
When challenged by hypertonicity, dehydrated cells must recover their volume to survive. This process requires the phosphorylation-dependent regulation of SLC12 cation chloride transporters by WNK kinases, but how these kinases are activated by cell shrinkage remains unknown. Within seconds of cell exposure to hypertonicity, WNK1 concentrates into membraneless condensates, initiating a phosphorylation-dependent signal that drives net ion influx via the SLC12 cotransporters to restore cell volume. WNK1 condensate formation is driven by its intrinsically disordered C terminus, whose evolutionarily conserved signatures are necessary for efficient phase separation and volume recovery. This disorder-encoded phase behavior occurs within physiological constraints and is activated in vivo by molecular crowding rather than changes in cell size. This allows kinase activity despite an inhibitory ionic milieu and permits cell volume recovery through condensate-mediated signal amplification. Thus, WNK kinases are physiological crowding sensors that phase separate to coordinate a cell volume rescue response.
