Polysialic acid as a regulator of intramuscular nerve branching during embryonic development

The role of polysialic acid (PSA) during initial innervation of chick muscle was examined. Previously, the adhesion molecules L1 and N-CAM were shown to be important in balancing axon-axon and axon-muscle adhesion during this process. Here we demonstrate developmental changes in the pattern of innervation that are not correlated with levels of L1 or N-CAM expression, but rather with the amount of PSA at the axon surface. Removal of PSA by a specific endoneuraminidase (Endo-N) increased axon fasciculation and reduced nerve branching. In contrast, the nerve trunk defasciculation and increased branching produced by neuromuscular activity blockade were associated with an increase in axonal PSA levels. Furthermore, Endo-N prevented these inactivity-induced effects on branching. Together these results illustrate the potential of PSA as a regulator of cell-cell interactions and provide a direct example of a molecular link between the morphogenic effects of adhesion-mediated and synaptic activity-dependent processes.     

The relationship of intramuscular nerve branching and synaptogenesis to motoneuron survival

The target has been considered for some time to play a major role in allowing neurons to survive the period of naturally occurring cell death. For the motoneurons that innervate the chick limb, evidence is presented that suggests access to target-derived trophic factor via intramuscular nerve branches and synapses may be important in regulating neuronal survival. Alterations in branching and synapse formation produced by activity blockade as well as by alteration of adhesion molecule function are shown to result in changes in motoneuron survival consistent with the proposed hypothesis. The relevance of these observations to the numerical-matching hypothesis of vertebrate neuronal cell death is also considered. © 1992 John Wiley & Sons, Inc.     

The relationship of intramuscular nerve branching and synaptogenesis to motoneuron survival.

The target has been considered for some time to play a major role in allowing neurons to survive the period of naturally occurring cell death. For the motoneurons that innervate the chick limb, evidence is presented that suggests access to target-derived trophic factor via intramuscular nerve branches and synapses may be important in regulating neuronal survival. Alterations in branching and synapse formation produced by activity blockade as well as by alteration of adhesion molecule function are shown to result in changes in motoneuron survival consistent with the proposed hypothesis. The relevance of these observations to the numerical-matching hypothesis of vertebrate neuronal cell death is also considered.     

Connectivity of identified central synapses in the cricket is normal following regeneration and blockade of presynaptic activity

Cercal sensory neurons in the cricket innervate interneurons in the central nervous system (CNS) and provide a model system for studying the formation of central synapses. When axons of the sensory neurons were transected during larval development, the cell bodies and the soma-bearing portion of axons, which are located within the cercus, survived but lost their excitability for 9-10 days. During this period, the sensory neurons grew new axons and reinnervated the terminal abdominal ganglion. Physiological recordings showed that sensory neurons of known identity reestablished monosynaptic contacts with their normal postsynaptic interneuron. Moreover, each synapse exhibited a characteristic strength indistinguishable from the intact synapse in an unoperated cricket. Since this selective connectivity was apparent immediately after the excitability of the axotomized sensory neurons was restored, action potentials in the sensory neurons appear to be unnecessary for normal synaptic regeneration to occur. Consistent with this, the reinnervation process was unaffected even when action potentials in the sensory neurons were blocked by tetrodotoxin (TTX) immediately following axotomy until just before testing. During the normal course of development, the characteristic strength of individual synapses changes systematically, resulting in the developmental rearrangement of these synapses (Chiba et al., 1988). This synaptic rearrangement was also unaffected when action potentials in the sensory neurons were blocked by TTX for the last 30% of larval development. Therefore, in the cricket cercal sensory system, both regeneration of the central synapses following axotomy of the presynaptic sensory neurons and the normal rearrangement of connectivity during larval development appear not to require axonal action potentials.     

The molecular and genetic regulation of shoot branching

The architecture of flowering plants exhibits both phenotypic diversity and plasticity, determined, in part, by the number and activity of axillary meristems and, in part, by the growth characteristics of the branches that develop from the axillary buds. The plasticity of shoot branching results from a combination of various intrinsic and genetic elements, such as number and position of nodes and type of growth phase, as well as environmental signals such as nutrient availability, light characteristics, and temperature (Napoli et al., 1998; Bennett and Leyser, 2006; Janssen et al., 2014; Teichmann and Muhr, 2015; Ueda and Yanagisawa, 2019). Axillary meristem initiation and axillary bud outgrowth are controlled by a complex and interconnected regulatory network. Although many of the genes and hormones that modulate branching patterns have been discovered and characterized through genetic and biochemical studies, there are still many gaps in our understanding of the control mechanisms at play. In this review, we will summarize our current knowledge of the control of axillary meristem initiation and outgrowth into a branch.

The key regulatory genes and the role of multiple plant hormones coordinate the process of axillary meristem initiation and subsequent growth into a branch.     

Carotid baroreflex regulation of sympathetic nerve activity during dynamic exercise in humans

We sought to determine whether carotid baroreflex (CBR) control of muscle sympathetic nerve activity (MSNA) was altered during dynamic exercise. In five men and three women, 23.8 +/- 0.7 (SE) yr of age, CBR function was evaluated at rest and during 20 min of arm cycling at 50% peak O(2) uptake using 5-s periods of neck pressure and neck suction. From rest to steady-state arm cycling, mean arterial pressure (MAP) was significantly increased from 90.0 +/- 2.7 to 118.7 +/- 3.6 mmHg and MSNA burst frequency (microneurography at the peroneal nerve) was elevated by 51 +/- 14% (P < 0.01). However, despite the marked increases in MAP and MSNA during exercise, CBR-Delta%MSNA responses elicited by the application of various levels of neck pressure and neck suction ranging from +45 to -80 Torr were not significantly different from those at rest. Furthermore, estimated baroreflex sensitivity for the control of MSNA at rest was the same as during exercise (P = 0.74) across the range of neck chamber pressures. Thus CBR control of sympathetic nerve activity appears to be preserved during moderate-intensity dynamic exercise.     

Tissue-dependent regulation of protein tyrosine kinase activity during embryonic development

Protein tyrosine kinase activity was assayed in a variety of chicken tissues during embryonic development and in the adult. In some tissues protein tyrosine kinase activity decreased during embryonic development; however, in other tissues it remained high throughout development, it contrast to the level of protein tyrosine phosphorylation, which decreased during development. The highest levels of tyrosine kinase activity were detected in 17-d embryonic brain although only low levels of protein tyrosine phosphorylation were observed in this tissue. Several alternatives were examined in an effort to determine the mechanism responsible for the low levels of tyrosine phosphorylated proteins in most older embryonic and adult chicken tissues despite the presence of highly active tyrosine kinases. The results show that the regulation of protein tyrosine phosphorylation during embryonic development is complex and varies from tissue to tissue. Furthermore, the results suggest that protein tyrosine phosphatases play an important role in regulating the level of phosphotyrosine in proteins of many older embryonic and adult tissues.     

The regulation of DNA repair during development

DNA repair is important in such phenomena as carcinogenesis and aging. While much is known about DNA repair in single-cell systems such as bacteria, yeast, and cultured mammalian cells, it is necessary to examine DNA repair in a developmental context in order to completely understand its processes in complex metazoa such as man. We present data to support the notion that proliferating cells from organ systems, tumors, and embryos have a greater DNA repair capacity than terminally differentiated, nonproliferating cells. Differential expression of repair genes and accessibility of chromatin to repair enzymes are considered as determinants in the developmental regulation of DNA repair.     

Temporal regulation of apterous activity during development of the Drosophila wing

Dorsoventral axis formation in the Drosophila wing depends on the activity of the selector gene apterous. Although selector genes are usually thought of as binary developmental switches, we find that Apterous activity is negatively regulated during wing development by its target gene dLMO. Apterous-dependent expression of Serrate and fringe in dorsal cells leads to the restricted activation of Notch along the dorsoventral compartment boundary. We present evidence that the ability of cells to participate in this Apterous-dependent cell-interaction is under spatial and temporal control. Apterous-dependent expression of dLMO causes downregulation of Serrate and fringe and allows expression of delta in dorsal cells. This limits the time window during which dorsoventral cell interactions can lead to localized activation of Notch and induction of the dorsoventral organizer. Overactivation of Apterous in the absence of dLMO leads to overexpression of Serrate, reduced expression of delta and concomitant defects in differentiation and cell survival in the wing primordium. Thus, downregulation of Apterous activity is needed to allow normal wing development.