Rho GTPase signaling and mDia facilitate endocytosis via presynaptic actin DOI Creative Commons
Kristine Oevel,

Svea Hohensee,

Atul Kumar

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2023, Номер unknown

Опубликована: Окт. 16, 2023

ABSTRACT Neurotransmission at synapses is mediated by the fusion and subsequent endocytosis of synaptic vesicle membranes. Actin has been suggested to be required for presynaptic but mechanisms that control actin polymerization its mode action within nerve terminals remain poorly understood. We combine optical recordings membrane dynamics ultrastructural analysis with genetic pharmacological manipulations demonstrate controlled regulatory diaphanous-related formins mDia1/3 Rho family GTPase signaling. show impaired assembly in near absence reduced RhoA activity partly compensated hyperactivation Rac1. Inhibition Rac1 signaling further aggravates elicited loss mDia1/3. Our data suggest interdependent mDia1/3-Rho pathways cooperatively act facilitate controlling F-actin.

Язык: Английский

Super-resolution imaging of the neuronal cytoskeleton DOI Creative Commons
Ciarán Butler-Hallissey, Christophe Leterrier

npj Imaging, Год журнала: 2024, Номер 2(1)

Опубликована: Дек. 4, 2024

Язык: Английский

Процитировано

0
Rho GTPase signaling and mDia facilitate endocytosis via presynaptic actin DOI Creative Commons
Kristine Oevel,

Svea Hohensee,

Atul Kumar

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2023, Номер unknown

Опубликована: Окт. 16, 2023

ABSTRACT Neurotransmission at synapses is mediated by the fusion and subsequent endocytosis of synaptic vesicle membranes. Actin has been suggested to be required for presynaptic but mechanisms that control actin polymerization its mode action within nerve terminals remain poorly understood. We combine optical recordings membrane dynamics ultrastructural analysis with genetic pharmacological manipulations demonstrate controlled regulatory diaphanous-related formins mDia1/3 Rho family GTPase signaling. show impaired assembly in near absence reduced RhoA activity partly compensated hyperactivation Rac1. Inhibition Rac1 signaling further aggravates elicited loss mDia1/3. Our data suggest interdependent mDia1/3-Rho pathways cooperatively act facilitate controlling F-actin.

Язык: Английский

Процитировано

0