The specificity of motor innervation of the chick wing does not depend upon the segmental origin of muscles

Development ◽  
1987 ◽  
Vol 99 (4) ◽  
pp. 565-575 ◽  
Author(s):  
R.J. Keynes ◽  
R.V. Stirling ◽  
C.D. Stern ◽  
D. Summerbell

In vertebrate embryos, motor axons originating from a particular craniocaudal position in the neural tube innervate limb muscles derived from myoblasts of the same segmental level. We have investigated whether this relationship is important for the formation of specific nerve-muscle connections, by altering the segmental origin of muscles and examining their resulting innervation. First, by grafting quail wing somites to a new craniocaudal position opposite the chick wing, we established that the segmental origin of a muscle can be altered: presumptive muscle cells migrated according to their new, rather than their original, somitic level, colonizing a different subset of muscles. However, after reversal of a length of brachial somitic mesoderm along the craniocaudal axis, or exchange or shift of brachial somites, the craniocaudal position of wing muscle motoneurone pools within the spinal cord was undisturbed, despite the new segmental origin of the muscles themselves. While not excluding the possibility that muscles and their motor nerves are labelled segmentally, we conclude that specific motor axon guidance in the wing does not depend upon the existence of such labels.

F1000Research ◽  
2014 ◽  
Vol 3 ◽  
pp. 275
Author(s):  
Chaya Kalcheim ◽  
Kate G. Storey

Mesodermal and spinal cord progenitors originate from common founder cells from which they segregate during development. Moreover, neural and mesodermal tissues closely interact during embryogenesis to ensure timely patterning and differentiation of both head and trunk structures. For instance, the fate and morphogenesis of neural progenitors is dependent on signals produced by mesodermal cells and vice-versa. While some of the cellular and molecular signals that mediate these interactions have been described, much more remains to be uncovered. The scope of this collection will cover these interactions between neural (CNS or PNS) and mesodermal progenitors in patterning body plans and specific body systems in vertebrate embryos. This includes, but is not limited to, interactions influencing the formation of body axes, neural tube formation, neural crest migration, gut development, muscle patterning and myogenesis.


Development ◽  
1999 ◽  
Vol 126 (8) ◽  
pp. 1665-1674 ◽  
Author(s):  
A.G. Borycki ◽  
J. Li ◽  
F. Jin ◽  
C.P. Emerson ◽  
J.A. Epstein

In developing vertebrate embryos, Pax3 is expressed in the neural tube and in the paraxial mesoderm that gives rise to skeletal muscles. Pax3 mutants develop muscular and neural tube defects; furthermore, Pax3 is essential for the proper activation of the myogenic determination factor gene, MyoD, during early muscle development and PAX3 chromosomal translocations result in muscle tumors, providing evidence that Pax3 has diverse functions in myogenesis. To investigate the specific functions of Pax3 in development, we have examined cell survival and gene expression in presomitic mesoderm, somites and neural tube of developing wild-type and Pax3 mutant (Splotch) mouse embryos. Disruption of Pax3 expression by antisense oligonucleotides significantly impairs MyoD activation by signals from neural tube/notochord and surface ectoderm in cultured presomitic mesoderm (PSM), and is accompanied by a marked increase in programmed cell death. In Pax3 mutant (Splotch) embryos, MyoD is activated normally in the hypaxial somite, but MyoD-expressing cells are disorganized and apoptosis is prevalent in newly formed somites, but not in the neural tube or mature somites. In neural tube and somite regions where cell survival is maintained, the closely related Pax7 gene is upregulated, and its expression becomes expanded into the dorsal neural tube and somites, where Pax3 would normally be expressed. These results establish that Pax3 has complementary functions in MyoD activation and inhibition of apoptosis in the somitic mesoderm and in repression of Pax7 during neural tube and somite development.


Development ◽  
2001 ◽  
Vol 128 (21) ◽  
pp. 4371-4382 ◽  
Author(s):  
Benno Schindelholz ◽  
Matthias Knirr ◽  
Rahul Warrior ◽  
Kai Zinn

Receptor-linked protein tyrosine phosphatases (RPTPs) regulate axon guidance and synaptogenesis in Drosophila embryos and larvae. We describe DPTP52F, the sixth RPTP to be discovered in Drosophila. Our genomic analysis indicates that there are likely to be no additional RPTPs encoded in the fly genome. Five of the six Drosophila RPTPs have C. elegans counterparts, and three of the six are also orthologous to human RPTP subfamilies. DPTP52F, however, has no clear orthologs in other organisms. The DPTP52F extracellular domain contains five fibronectin type III repeats and it has a single phosphatase domain. DPTP52F is selectively expressed in the CNS of late embryos, as are DPTP10D, DLAR, DPTP69D and DPTP99A. To define developmental roles of DPTP52F, we used RNA interference (RNAi)-induced phenotypes as a guide to identify Ptp52F alleles among a collection of EMS-induced lethal mutations. Ptp52F single mutant embryos have axon guidance phenotypes that affect CNS longitudinal tracts. This phenotype is suppressed in Dlar Ptp52F double mutants, indicating that DPTP52F and DLAR interact competitively in regulating CNS axon guidance decisions. Ptp52F single mutations also cause motor axon phenotypes that selectively affect the SNa nerve. DPTP52F, DPTP10D and DPTP69D have partially redundant roles in regulation of guidance decisions made by axons within the ISN and ISNb motor nerves.


2021 ◽  
Author(s):  
Yi‐Syue Tsou ◽  
Chih‐Yang Wang ◽  
Ming‐Yuan Chang ◽  
Tsung‐I Hsu ◽  
Meng‐Ting Wu ◽  
...  

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