The autonomous axon: a model based on local synthesis of proteins.
In the current understanding of axons, axoplasmic synthesis of proteins is negated, and it is asserted that proteins are transported from perikarya to axons. This 'transport model' in which axons are fully dependent of perikarya is seriously flawed. The 'autonomous axon' proposed here negates in turn transport of proteins, and asserts (i) local synthesis of axoplasmic proteins, corner stone of this model, (ii) existence of internal programs in axon and terminals, (iii) external control of programs resulting in local regulation of phenotype of axons and terminals, hence they are autonomous from perikarya; (iv) participation of perikarya through the fast transport in setting up the axonal programs but not in their immediate regulation. The word merotrophism (meros meaning part) denotes post-transcriptional regulation of phenotype of restricted regions of a cell. We surmise that merotrophism is at the base of many plastic phenomena.
Alvarez
J
J
Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Casilla 114-D, Santiago, Chile. jalvarez@genes.bio.puc.cl
D000818:Animals; D001370:Axonal Transport; D001369:Axons / Q000502:physiology*; D001692:Biological Transport; D006801:Humans; D008959:Models, Neurological; D009419:Nerve Tissue Proteins / Q000096:biosynthesis*; D017729:Presynaptic Terminals / Q000502:physiology; D012270:Ribosomes / Q000378:metabolism; D012583:Schwann Cells / Q000502:physiology
D009419:Nerve Tissue Proteins