Faculty Opinions recommendation of A Neuronal piRNA Pathway Inhibits Axon Regeneration in C. elegans.

2018 ◽  
Author(s):  
Peter Boag
Keyword(s):  
Axon Regeneration ◽  
C Elegans ◽  
Pirna Pathway

scholarly journals A Neuronal piRNA Pathway Inhibits Axon Regeneration in C. elegans

Neuron ◽  
2018 ◽  
Vol 97 (3) ◽  
pp. 511-519.e6 ◽  
Author(s):  
Kyung Won Kim ◽  
Ngang Heok Tang ◽  
Matthew G. Andrusiak ◽  
Zilu Wu ◽  
Andrew D. Chisholm ◽  
...  
Keyword(s):  
Axon Regeneration ◽  
C Elegans ◽  
Pirna Pathway

scholarly journals rab-27 acts in an intestinal pathway to inhibit axon regeneration in C. elegans

PLoS Genetics ◽  
2021 ◽  
Vol 17 (11) ◽  
pp. e1009877
Author(s):  
Alexander T. Lin-Moore ◽  
Motunrayo J. Oyeyemi ◽  
Marc Hammarlund
Keyword(s):  
Motor Neurons ◽  
Axon Regeneration ◽  
Rab Gtpase ◽  
Long Distance ◽  
Extrinsic Factors ◽  
C Elegans ◽  
Cellular Environment ◽  
Neuropeptide Secretion ◽  
Neuronal Tissues ◽  
Nervous System Function

Injured axons must regenerate to restore nervous system function, and regeneration is regulated in part by external factors from non-neuronal tissues. Many of these extrinsic factors act in the immediate cellular environment of the axon to promote or restrict regeneration, but the existence of long-distance signals regulating axon regeneration has not been clear. Here we show that the Rab GTPase rab-27 inhibits regeneration of GABAergic motor neurons in C. elegans through activity in the intestine. Re-expression of RAB-27, but not the closely related RAB-3, in the intestine of rab-27 mutant animals is sufficient to rescue normal regeneration. Several additional components of an intestinal neuropeptide secretion pathway also inhibit axon regeneration, including NPDC1/cab-1, SNAP25/aex-4, KPC3/aex-5, and the neuropeptide NLP-40, and re-expression of these genes in the intestine of mutant animals is sufficient to restore normal regeneration success. Additionally, NPDC1/cab-1 and SNAP25/aex-4 genetically interact with rab-27 in the context of axon regeneration inhibition. Together these data indicate that RAB-27-dependent neuropeptide secretion from the intestine inhibits axon regeneration, and point to distal tissues as potent extrinsic regulators of regeneration.

scholarly journals CELF RNA binding proteins promote axon regeneration in C. elegans and mammals through alternative splicing of Syntaxins

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Lizhen Chen ◽  
Zhijie Liu ◽  
Bing Zhou ◽  
Chaoliang Wei ◽  
Yu Zhou ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcriptional Regulation ◽  
Alternative Splicing ◽  
Binding Proteins ◽  
Rna Binding ◽  
Axon Regeneration ◽  
Rna Binding Proteins ◽  
Mrna Isoforms ◽  
C Elegans ◽  
Mrna Targets

Axon injury triggers dramatic changes in gene expression. While transcriptional regulation of injury-induced gene expression is widely studied, less is known about the roles of RNA binding proteins (RBPs) in post-transcriptional regulation during axon regeneration. In C. elegans the CELF (CUGBP and Etr-3 Like Factor) family RBP UNC-75 is required for axon regeneration. Using crosslinking immunoprecipitation coupled with deep sequencing (CLIP-seq) we identify a set of genes involved in synaptic transmission as mRNA targets of UNC-75. In particular, we show that UNC-75 regulates alternative splicing of two mRNA isoforms of the SNARE Syntaxin/unc-64. In C. elegans mutants lacking unc-75 or its targets, regenerating axons form growth cones, yet are deficient in extension. Extending these findings to mammalian axon regeneration, we show that mouse Celf2 expression is upregulated after peripheral nerve injury and that Celf2 mutant mice are defective in axon regeneration. Further, mRNAs for several Syntaxins show CELF2 dependent regulation. Our data delineate a post-transcriptional regulatory pathway with a conserved role in regenerative axon extension.

scholarly journals Effects of NAD+ in Caenorhabditis elegans Models of Neuronal Damage

Biomolecules ◽  
2020 ◽  
Vol 10 (7) ◽  
pp. 993
Author(s):  
Yuri Lee ◽  
Hyeseon Jeong ◽  
Kyung Hwan Park ◽  
Kyung Won Kim
Keyword(s):  
Caenorhabditis Elegans ◽  
Therapeutic Strategy ◽  
Axon Regeneration ◽  
Neuronal Damage ◽  
Biological Processes ◽  
Nematode Caenorhabditis Elegans ◽  
C Elegans ◽  
Neuronal Functions ◽  
Molecular Components

Nicotinamide adenine dinucleotide (NAD+) is an essential cofactor that mediates numerous biological processes in all living cells. Multiple NAD+ biosynthetic enzymes and NAD+-consuming enzymes are involved in neuroprotection and axon regeneration. The nematode Caenorhabditis elegans has served as a model to study the neuronal role of NAD+ because many molecular components regulating NAD+ are highly conserved. This review focuses on recent findings using C. elegans models of neuronal damage pertaining to the neuronal functions of NAD+ and its precursors, including a neuroprotective role against excitotoxicity and axon degeneration as well as an inhibitory role in axon regeneration. The regulation of NAD+ levels could be a promising therapeutic strategy to counter many neurodegenerative diseases, as well as neurotoxin-induced and traumatic neuronal damage.

scholarly journals Functional Dissection of C. elegans bZip-Protein CEBP-1 Reveals Novel Structural Motifs Required for Axon Regeneration and Nuclear Import

2019 ◽  
Vol 13 ◽  
Author(s):  
Rose Aria Malinow ◽  
Phoenix Ying ◽  
Thijs Koorman ◽  
Mike Boxem ◽  
Yishi Jin ◽  
...  
Keyword(s):  
Nuclear Import ◽  
Axon Regeneration ◽  
Structural Motifs ◽  
Bzip Protein ◽  
C Elegans

scholarly journals Axon regeneration mechanisms: insights from C. elegans

2011 ◽  
Vol 21 (10) ◽  
pp. 577-584 ◽  
Author(s):  
Lizhen Chen ◽  
Andrew D. Chisholm
Keyword(s):  
Axon Regeneration ◽  
C Elegans

scholarly journals The C. elegans peroxidasin PXN-2 is essential for embryonic morphogenesis and inhibits adult axon regeneration

Development ◽  
2010 ◽  
Vol 137 (21) ◽  
pp. 3603-3613 ◽  
Author(s):  
J. R. Gotenstein ◽  
R. E. Swale ◽  
T. Fukuda ◽  
Z. Wu ◽  
C. A. Giurumescu ◽  
...  
Keyword(s):  
Axon Regeneration ◽  
C Elegans ◽  
Embryonic Morphogenesis

scholarly journals rab-27 acts in an intestinal secretory pathway to inhibit axon regeneration in C. elegans

2020 ◽  
Author(s):  
Alexander T. Lin-Moore ◽  
Motunrayo J. Oyeyemi ◽  
Marc Hammarlund
Keyword(s):  
Motor Neurons ◽  
Secretory Pathway ◽  
Axon Regeneration ◽  
Rab Gtpase ◽  
Long Distance ◽  
Extrinsic Factors ◽  
C Elegans ◽  
Cellular Environment ◽  
Neuropeptide Secretion ◽  
Neuronal Tissues

ABSTRACTInjured axons must regenerate to restore nervous system function, and regeneration is regulated in part by external factors from non-neuronal tissues. Many of these extrinsic factors act in the immediate cellular environment of the axon to promote or restrict regeneration, but the existence of long-distance signals regulating axon regeneration has not been clear. Here we show that the Rab GTPase rab-27 inhibits regeneration of GABAergic motor neurons in C. elegans through activity in the intestine. Re-expression of RAB-27, but not the closely related RAB-3, in the intestine of rab-27 mutant animals is sufficient to rescue normal regeneration. Several additional components of an intestinal neuropeptide secretion pathway also inhibit axon regeneration, including NPDC1/cab-1, SNAP25/aex-4, and KPC3/aex-5. Together these data indicate that RAB-27-dependent neuropeptide secretion from the intestine inhibits axon regeneration, and point to distal tissues as potent extrinsic regulators of regeneration.

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