scholarly journals Opposing functions of F-BAR proteins in neuronal membrane protrusion, tubule formation, and neurite outgrowth

2019 ◽  
Vol 2 (3) ◽  
pp. e201800288 ◽  
Author(s):  
Kendra L Taylor ◽  
Russell J Taylor ◽  
Karl E Richters ◽  
Brandon Huynh ◽  
Justin Carrington ◽  
...  
Keyword(s):  
Neurite Outgrowth ◽  
Cortical Neurons ◽  
Neuronal Development ◽  
Actin Dynamics ◽  
Neuronal Membrane ◽  
Membrane Protrusion ◽  
Tubule Formation ◽  
Primary Cortical Neurons ◽  
Splice Isoforms ◽  
Neurite Formation

The F-BAR family of proteins play important roles in many cellular processes by regulating both membrane and actin dynamics. The CIP4 family of F-BAR proteins is widely recognized to function in endocytosis by elongating endocytosing vesicles. However, in primary cortical neurons, CIP4 concentrates at the tips of extending lamellipodia and filopodia and inhibits neurite outgrowth. Here, we report that the highly homologous CIP4 family member, FBP17, induces tubular structures in primary cortical neurons and results in precocious neurite formation. Through domain swapping and deletion experiments, we demonstrate that a novel polybasic region between the F-BAR and HR1 domains is required for membrane bending. Moreover, the presence of a poly-PxxP region in longer splice isoforms of CIP4 and FBP17 largely reverses the localization and function of these proteins. Thus, CIP4 and FBP17 function as an antagonistic pair to fine-tune membrane protrusion, endocytosis, and neurite formation during early neuronal development.

scholarly journals Lin28 overexpression inhibits neurite outgrowth of primary cortical neurons in vitro

2018 ◽  
Vol 78 (4) ◽  
pp. 297-304
Author(s):  
Mohammad Iqbal Hossain Bhuiyan ◽  
Seong Yun Kim ◽  
Kyung-Ok Cho
Keyword(s):  
Neurite Outgrowth ◽  
Cortical Neurons ◽  
Primary Cortical Neurons

scholarly journals Cofilin and Actin Dynamics: Multiple Modes of Regulation and Their Impacts in Neuronal Development and Degeneration

Cells ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 2726
Author(s):  
James R. Bamburg ◽  
Laurie S. Minamide ◽  
O’Neil Wiggan ◽  
Lubna H. Tahtamouni ◽  
Thomas B. Kuhn
Keyword(s):  
Cortical Neurons ◽  
Hippocampal Neurons ◽  
Translational Regulation ◽  
Neuronal Development ◽  
Mitochondrial Fission ◽  
Amyloid Β ◽  
Cellular Prion Protein ◽  
Actin Dynamics ◽  
Specific Regulation ◽  
And Function

Proteins of the actin depolymerizing factor (ADF)/cofilin family are ubiquitous among eukaryotes and are essential regulators of actin dynamics and function. Mammalian neurons express cofilin-1 as the major isoform, but ADF and cofilin-2 are also expressed. All isoforms bind preferentially and cooperatively along ADP-subunits in F-actin, affecting the filament helical rotation, and when either alone or when enhanced by other proteins, promotes filament severing and subunit turnover. Although self-regulating cofilin-mediated actin dynamics can drive motility without post-translational regulation, cells utilize many mechanisms to locally control cofilin, including cooperation/competition with other proteins. Newly identified post-translational modifications function with or are independent from the well-established phosphorylation of serine 3 and provide unexplored avenues for isoform specific regulation. Cofilin modulates actin transport and function in the nucleus as well as actin organization associated with mitochondrial fission and mitophagy. Under neuronal stress conditions, cofilin-saturated F-actin fragments can undergo oxidative cross-linking and bundle together to form cofilin-actin rods. Rods form in abundance within neurons around brain ischemic lesions and can be rapidly induced in neurites of most hippocampal and cortical neurons through energy depletion or glutamate-induced excitotoxicity. In ~20% of rodent hippocampal neurons, rods form more slowly in a receptor-mediated process triggered by factors intimately connected to disease-related dementias, e.g., amyloid-β in Alzheimer’s disease. This rod-inducing pathway requires a cellular prion protein, NADPH oxidase, and G-protein coupled receptors, e.g., CXCR4 and CCR5. Here, we will review many aspects of cofilin regulation and its contribution to synaptic loss and pathology of neurodegenerative diseases.

Sonic Hedgehog Promotes Neurite Outgrowth of Primary Cortical Neurons Through Up-Regulating BDNF Expression

2015 ◽  
Vol 41 (4) ◽  
pp. 687-695 ◽  
Author(s):  
Weiliang He ◽  
Lili Cui ◽  
Cong Zhang ◽  
Xiangjian Zhang ◽  
Junna He ◽  
...  
Keyword(s):  
Neurite Outgrowth ◽  
Sonic Hedgehog ◽  
Cortical Neurons ◽  
Bdnf Expression ◽  
Primary Cortical Neurons

Noradrenaline acting on astrocytic β2-adrenoceptors induces neurite outgrowth in primary cortical neurons

2014 ◽  
Vol 77 ◽  
pp. 234-248 ◽  
Author(s):  
Jennifer S. Day ◽  
Eimear O'Neill ◽  
Caroline Cawley ◽  
Nicholas Kruseman Aretz ◽  
Dana Kilroy ◽  
...  
Keyword(s):  
Neurite Outgrowth ◽  
Cortical Neurons ◽  
Primary Cortical Neurons

scholarly journals Docosahexanoic acid signals through the Nrf2–Nqo1 pathway to maintain redox balance and promote neurite outgrowth

2021 ◽  
pp. mbc.E20-09-0599
Author(s):  
Jennifer Drolet ◽  
Brodie Buchner-Duby ◽  
Morgan G. Stykel ◽  
Carla Coackley ◽  
Jing X. Kang ◽  
...  
Keyword(s):  
Neurite Outgrowth ◽  
Cortical Neurons ◽  
Target Gene ◽  
Neuronal Development ◽  
Redox Balance ◽  
Antioxidant Response ◽  
Neuronal Projection ◽  
Nrf2 Target Gene ◽  
Significant Enrichment ◽  
Quinone Acceptor

Evidence suggests that n-3 polyunsaturated fatty acids (PUFA) may act as activators of the Nrf2 antioxidant pathway. The antioxidant response in-turn promotes neuronal differentiation and neurite outgrowth. Nrf2 has recently been suggested to be a cell intrinsic mediator of DHA signaling. In the current study, we assessed whether DHA mediated axodendritic development was dependent on activation of the Nrf2-pathway and whether Nrf2 protected from agrochemical-induced neuritic retraction. Expression profiling of the DHA-enriched Fat-1 mouse brain relative to WT showed a significant enrichment of genes associated with neuronal development and neuronal projection and genes associated with the Nrf2-transcriptional pathway. Moreover, we found that primary cortical neurons treated with DHA showed a dose dependent increase in Nrf2 transcriptional activity and Nrf2-target gene expression. DHA-mediated activation of Nrf2 promoted neurite outgrowth and inhibited oxidative stress induced neuritic retraction evoked by exposure to agrochemicals. Finally, we provide evidence that this effect is largely dependent on induction of the Nrf2-target gene NAD(P)H: (quinone acceptor) oxidoreductase 1 (NQO1), and that silencing of either Nrf2 or Nqo1 blocks the effects of DHA on the axodendritic compartment. Collectively, these data support a role for the Nrf2-NQO1 pathway in DHA-mediated axodendritic development and protection from agrochemical exposure.

scholarly journals hnRNP-Q1 represses nascent axon growth in cortical neurons by inhibitingGap-43mRNA translation

2016 ◽  
Vol 27 (3) ◽  
pp. 518-534 ◽  
Author(s):  
Kathryn R. Williams ◽  
Damian S. McAninch ◽  
Snezana Stefanovic ◽  
Lei Xing ◽  
Megan Allen ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Posttranscriptional Regulation ◽  
Neuronal Development ◽  
Regulation Of Gene Expression ◽  
Axon Growth ◽  
Mrna Translation ◽  
Actin Dynamics ◽  
Neuro2a Cell ◽  
And Function ◽  
Mrna Binding

Posttranscriptional regulation of gene expression by mRNA-binding proteins is critical for neuronal development and function. hnRNP-Q1 is an mRNA-binding protein that regulates mRNA processing events, including translational repression. hnRNP-Q1 is highly expressed in brain tissue, suggesting a function in regulating genes critical for neuronal development. In this study, we have identified Growth-associated protein 43 (Gap-43) mRNA as a novel target of hnRNP-Q1 and have demonstrated that hnRNP-Q1 represses Gap-43 mRNA translation and consequently GAP-43 function. GAP-43 is a neuronal protein that regulates actin dynamics in growth cones and facilitates axonal growth. Previous studies have identified factors that regulate Gap-43 mRNA stability and localization, but it remains unclear whether Gap-43 mRNA translation is also regulated. Our results reveal that hnRNP-Q1 knockdown increased nascent axon length, total neurite length, and neurite number in mouse embryonic cortical neurons and enhanced Neuro2a cell process extension; these phenotypes were rescued by GAP-43 knockdown. Additionally, we have identified a G-quadruplex structure in the 5′ untranslated region of Gap-43 mRNA that directly interacts with hnRNP-Q1 as a means to inhibit Gap-43 mRNA translation. Therefore hnRNP-Q1–mediated repression of Gap-43 mRNA translation provides an additional mechanism for regulating GAP-43 expression and function and may be critical for neuronal development.

scholarly journals Electrical Stimulation with a Conductive Polymer Promotes Neurite Outgrowth and Synaptogenesis in Primary Cortical Neurons in 3D

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Qingsheng Zhang ◽  
Stephen Beirne ◽  
Kewei Shu ◽  
Dorna Esrafilzadeh ◽  
Xu-Feng Huang ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Neurite Outgrowth ◽  
Cortical Neurons ◽  
Conductive Polymer ◽  
Primary Cortical Neurons
Sign in / Sign up

Export Citation Format

Share Document