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Chromatolysis: Do injured axons regenerate poorly when ribonucleases attack rough endoplasmic reticulum, ribosomes and RNA?
Developmental neurobiology (Hoboken, N.J.), 2018-10, Vol.78 (10), p.1011-1024
Moon, Lawrence David Falcon
2018
Volltextzugriff (PDF)
Details
Autor(en) / Beteiligte
Moon, Lawrence David Falcon
Titel
Chromatolysis: Do injured axons regenerate poorly when ribonucleases attack rough endoplasmic reticulum, ribosomes and RNA?
Ist Teil von
Developmental neurobiology (Hoboken, N.J.), 2018-10, Vol.78 (10), p.1011-1024
Ort / Verlag
United States: Wiley Subscription Services, Inc
Erscheinungsjahr
2018
Quelle
Wiley Online Library All Journals
Beschreibungen/Notizen
ABSTRACT After axonal injury, chromatolysis (fragmentation of Nissl substance) can occur in the soma. Electron microscopy shows that chromatolysis involves fission of the rough endoplasmic reticulum. In CNS neurons (which do not regenerate axons back to their original targets) or in motor neurons or dorsal root ganglion neurons denied axon regeneration (e.g., by transection and ligation), chromatolysis is often accompanied by degranulation (loss of ribosomes from rough endoplasmic reticulum), disaggregation of polyribosomes and degradation of monoribosomes into dust‐like particles. Ribosomes and rough endoplasmic reticulum may also be degraded in autophagic vacuoles by ribophagy and reticulophagy, respectively. In other words, chromatolysis is disruption of parts of the protein synthesis infrastructure. Whereas some neurons may show transient or no chromatolysis, severely injured neurons can remain chromatolytic and never again synthesize normal levels of protein; some may atrophy or die. Ribonuclease(s) might cause the following features of chromatolysis: fragmentation and degranulation of rough endoplasmic reticulum, disaggregation of polyribosomes and degradation of monoribosomes. For example, ribonucleases in the EndoU/PP11 family can modify rough endoplasmic reticulum; many ribonucleases can degrade mRNA causing polyribosomes to unchain and disperse, and they can disassemble monoribosomes; Ribonuclease 5 can control rRNA synthesis and degrade tRNA; Ribonuclease T2 can degrade ribosomes, endoplasmic reticulum and RNA within autophagic vacuoles; and Ribonuclease IRE1α acts as a stress sensor within the endoplasmic reticulum. Regeneration might be improved after axonal injury by protecting the protein synthesis machinery from catabolism; targeting ribonucleases using inhibitors can enhance neurite outgrowth and could be a profitable strategy in vivo. © 2018 Wiley Periodicals, Inc. Develop Neurobiol, 2018
Sprache
Englisch
Identifikatoren
ISSN: 1932-8451
eISSN: 1932-846X
DOI: 10.1002/dneu.22625
Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6334169
Format
–
Schlagworte
Angiogenin
,
Atrophy
,
Axon guidance
,
Axonogenesis
,
Axons
,
Catabolism
,
Central nervous system
,
chromatolysis
,
Degranulation
,
Disaggregation
,
Dismantling
,
Dorsal root ganglia
,
Electron microscopy
,
Endoplasmic reticulum
,
Fragmentation
,
Motor neurons
,
mRNA
,
Neurons
,
Polyribosomes
,
Protein biosynthesis
,
Protein synthesis
,
Proteins
,
Regeneration
,
Review
,
ribonuclease
,
Ribonuclease S
,
Ribonuclease T2
,
Ribonucleases
,
ribosome
,
Ribosomes
,
rRNA
,
tRNA
,
Vacuoles
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