Why adult mammalian intrafusal and extrafusal fibers contain different myosin heavy-chain isoforms.
*Muscle Development; Afferent Pathways/physiology; Aging/metabolism; Animals; Cell Lineage; Developmental; Fetal Proteins/metabolism; Gene Expression Regulation; Knockout; Mammals/anatomy & histology/*metabolism; Mice; Morphogenesis; Muscle; Muscle Contraction; Muscle Fibers; Muscle Proteins/deficiency/physiology; Muscle Spindles/physiology; Myosin Heavy Chains/*metabolism; Nerve Tissue Proteins/deficiency/physiology; Protein Isoforms/*metabolism; Rats; Skeletal/*chemistry/classification; Skeletal/chemistry/embryology/*growth & development/ultrastructure; Transgenic
Multiple isoforms of the contractile protein myosin are present in mammalian skeletal muscles. The diversity of the heavy-chain subunits of myosin (MyHCs) in intrafusal fibers is thought to reflect a pathway of differentiation that is unique to muscle spindles. In fact, intrafusal MyHCs are developmental isoforms expressed by the prenatal precursors of both intrafusal and extrafusal fibers. In adult limbs, developmental MyHCs persist in intrafusal, but not extrafusal fibers principally due to the afferent neurons that arrest their maturational replacement by MyHCs associated with faster shortening velocities. The slow shortening velocities that are characteristic of developmental MyHCs might be adaptive for precise calibration of muscle spindles as sense organs.
Walro J M; Kucera J
Trends in neurosciences
1999
1999-04
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/s0166-2236(98)01339-3" target="_blank" rel="noreferrer noopener">10.1016/s0166-2236(98)01339-3</a>
Stability of myosin heavy chain isoforms in selectively denervated adult rat muscle spindles.
Afferent/physiology; Animals; Efferent/physiology; Female; Ganglia; Muscle; Muscle Denervation; Muscle Fibers; Muscle Spindles/*enzymology; Myosin Heavy Chains/analysis/chemistry/*metabolism; Myosins/*metabolism; Neurons; Rats; Skeletal/*enzymology/ultrastructure; Skeletal/cytology/enzymology/innervation; Spinal/surgery; Sprague-Dawley
BACKGROUND: Rat intrafusal fibers consist of multiple isoforms of myosin heavy chains (MHCs) whose expression involves complex interactions among motor neurons, sensory neurons, and muscle cells during spindle development. Little is known about the roles of sensory and motor innervation in regulating and maintaining expression of MHC isoforms in adult rat muscle spindles. METHODS: MHC expression was investigated in deafferented or deefferented adult rat muscle spindles by reacting transverse sections of spindles with a panel of monoclonal antibodies specific for different MHC isoforms. RESULTS: Deefferentation or deafferentation did not alter the number of intrafusal fibers expressing most MHC isoforms. However, the numbers of fibers expressing two MHC isoforms were altered in deefferented muscle spindles. Nuclear bag1 fibers ceased to express alpha-cardiac MHC and upregulated embryonic MHC after ablation of motor innervation. Likewise, bag2 and chain fibers downregulated avian neonatal/fast MHC following deafferentation, but chain fibers upregulated type 2A MHC and became more extrafusal-like in their pattern of MHC expression. CONCLUSIONS: These data indicate that (1) perturbations in spindle sensory and motor nerve supplies produce less severe alterations in MHC expression in mature intrafusal fibers than do similar lesions in developing intrafusal fibers and (2) MHC expression in intrafusal fibers reflects a combination of inductive and suppressive effects of motor and sensory neurons.
Wang J; McWhorter D L; Walro J M
The Anatomical record
1997
1997-09
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1002/(sici)1097-0185(199709)249:1%3C32::aid-ar5%3E3.0.co;2-h" target="_blank" rel="noreferrer noopener">10.1002/(sici)1097-0185(199709)249:1%3C32::aid-ar5%3E3.0.co;2-h</a>