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One of the earliest events in neuromuscular junction (NMJ) development is the accumulation of acetylcholine receptor (AChR) at the center of muscle cells. The unplugged/MuSK (muscle specific tyrosine kinase) gene is essential to initiate AChR clustering but also to restrict approaching growth cones to the muscle center, thereby coordinating pre- and postsynaptic development. To determine how unplugged/MuSK signaling coordinates these two processes, we examined the temporal and spatial requirements of unplugged/MuSK in zebrafish embryos using heat-shock inducible transgenes. Here, we show that despite its expression in muscle cells from the time they differentiate, unplugged/MuSK activity is first required just prior to the appearance of AChR clusters to simultaneously induce AChR accumulation and to guide motor axons. Furthermore, we demonstrate that ectopic expression of unplugged/MuSK throughout the muscle membrane results in wildtype-like AChR prepattern and neuromuscular synapses in the central region of muscle cells. We propose that AChR prepatterning and axonal guidance are spatio-temporally coordinated through common unplugged/MuSK signals, and that additional factor(s) restrict unplugged/MuSK signaling to a central muscle zone critical for establishing mid-muscle synaptogenesis. [ABSTRACT FROM AUTHOR]

One of the earliest events in neuromuscular junction (NMJ) development is the accumulation of acetylcholine receptor (AChR) at the center of muscle cells. The unplugged/MuSK (muscle specific tyrosine kinase) gene is essential to initiate AChR clustering but also to restrict approaching growth cones to the muscle center, thereby coordinating pre- and postsynaptic development. To determine how unplugged/MuSK signaling coordinates these two processes, we examined the temporal and spatial requirements of unplugged/MuSK in zebrafish embryos using heat-shock inducible transgenes. Here, we show that despite its expression in muscle cells from the time they differentiate, unplugged/MuSK activity is first required just prior to the appearance of AChR clusters to simultaneously induce AChR accumulation and to guide motor axons. Furthermore, we demonstrate that ectopic expression of unplugged/MuSK throughout the muscle membrane results in wildtype-like AChR prepattern and neuromuscular synapses in the central region of muscle cells. We propose that AChR prepatterning and axonal guidance are spatio-temporally coordinated through common unplugged/MuSK signals, and that additional factor(s) restrict unplugged/MuSK signaling to a central muscle zone critical for establishing mid-muscle synaptogenesis.

The title compound, poly[dizinc(II)-μ-ethylenediamine-di-μ-(hydrogen phosphito)], β-[H2N(CH2)2NH2]0.5[ZnHPO3] or [Zn2(HPO3)2(C2H–N–)]n, is a hybrid organic/inorganic solid built up from ethylenediamine molecules (which lie about inversion centres), Zn2+ cations (coordinated by three O atoms and one N atom) and HPO32- hydrogen phosphite groups. The organic species bond to the Zn atom as unprotonated ligands, acting as bridges between infinite ZnHPO3 layers that propagate as very buckled (001) sheets. The zincophosphite sheets contain polyhedral four- and eight-membered rings in a 4.82 topology, β-[H2N(CH2)2- NH2]0.5·ZnHPO3 complements the previously described α modification of the same stoichiometry [Rodgers & Harrison (2000). Chem. Commun. pp. 2385–2386]. [ABSTRACT FROM AUTHOR]

In this article the authors comment on Janet Hunt's review of their book "The Sociology of Gender." According to the authors, Hunt accurately presents the main themes of the book. However, Hunt misrepresents their work when she states that "gender is implied to be a less-significant barrier to power and privilege than social class and race." The authors do not imply this perspective, they take it, devoting considerable space to the explication of a complex reality and to presenting pertinent evidence. Here Hunt fails to discuss the substance of the text, focusing almost exclusively on questions of form. The question of how equalizing power will affect the stratification system, for example, cannot be answered simply or definitively. The authors maintain that the route by which power is equalized must be considered. Thus, their discussion of the diversity of feminist goals and strategies elaborates their different implications. The authors readily admit to being unable to describe the specific design of a feminist future. It is peculiar to expect them to resolve what have been among the central questions of feminist theory and politics throughout its history.

Trunk neural crest cells delaminate from the dorsal neural tube as an uninterrupted sheet; however, they convert into segmentally organized streams before migrating through the somitic territory. These neural crest cell streams join the segmental trajectories of pathfinding spinal motor axons, suggesting that interactions between these two cell types might be important for neural crest cell migration. Here, we show that in the zebrafish embryo migration of both neural crest cells and motor axons is temporally synchronized and spatially restricted to the center of the somite, but that motor axons are dispensable for segmental neural crest cell migration. Instead, we find that muscle-specific receptor kinase (MuSK) and its putative ligand Wnt11r are crucial for restricting neural crest cell migration to the center of each somite. Moreover, we find that blocking planar cell polarity (PCP) signaling in somitic muscle cells also results in non-segmental neural crest cell migration. Using an F-actin biosensor we show that in the absence of MuSK neural crest cells fail to retract non-productive leading edges, resulting in non-segmental migration. Finally, we show that MuSK knockout mice display similar neural crest cell migration defects, suggesting a novel, evolutionarily conserved role for MuSK in neural crest migration. We propose that a Wnt11r-MuSK dependent, PCP-like pathway restricts neural crest cells to their segmental path.

The title compound, poly[dizinc(II)-mu-ethylenediamine-di-mu-(hydrogen phosphito)], beta-[H(2)N(CH(2))(2)NH(2)](0.5)[ZnHPO(3)] or [Zn(2)(HPO(3))(2)(C(2)H(8)N(2))](n), is a hybrid organic/inorganic solid built up from ethylenediamine molecules (which lie about inversion centres), Zn(2+) cations (coordinated by three O atoms and one N atom) and HPO(3)(2-) hydrogen phosphite groups. The organic species bond to the Zn atom as unprotonated ligands, acting as bridges between infinite ZnHPO(3) layers that propagate as very buckled (001) sheets. The zincophosphite sheets contain polyhedral four- and eight-membered rings in a 4.8(2) topology. beta-[H(2)N(CH(2))(2)NH(2)](0.5).ZnHPO(3) complements the previously described alpha modification of the same stoichiometry [Rodgers & Harrison (2000). Chem. Commun. pp. 2385-2386].