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Neuromuscular junctions (NMJs) are peripheral synapses between motoneurons and skeletal muscle fibers that are critical for the control of muscle contraction. Dysfunction of these synapses has been implicated in congenital myasthenic syndrome (CMS). In vertebrates, agrin‐LRP4‐MuSK signaling plays a critical role in acetylcholine receptor (AChR) clustering and NMJ formation. The adaptor protein DOK7 is the downstream substrate of MuSK and also a cytoplasmic activator of MuSK. The role of DOK7 in the promotion of AChR clustering and the mechanisms involved have been well studied; however, the negative regulation of DOK7 after MuSK activation remains unknown. Anaphase‐promoting complex 2 (APC2), the core subunit of APC/C E3 ligase complex, was originally believed to regulate cell‐cycle transitions. Here, we show that APC2 is enriched at post‐synapse of NMJs in postmitotic myotubes. In response to agrin stimulation, APC2 negatively regulates AChR clustering by promoting the ubiquitination of DOK7 at lysine 243 for its proteolytic degradation, which relies on MuSK kinase activity and the phosphorylation of tyrosine 106 in DOK7. Thus, this study provides a mechanism whereby agrin signaling is negatively regulated as part of vertebrate NMJ homeostasis.

Quantitative Polymerase Chain Reaction (qPCR) has revolutionized the detection of DNA and RNA. But the quantification results are susceptible to the effects of background noise and the intensity of detected fluorescent signals. Aiming at solving the above problem, this paper presents a signal preamplifier circuit which is compatible to the fluorescence detection system. In the entire process of genetic quantification, the signal preamplifier circuit plays a very important role in amplifying the subtle fluorescent signal and eliminating the noise in the meantime. Experiment results show that with the help of this amplifier, the qPCR instrument can have a better performance in detecting weak fluorescent signals and precise quantification.

Bisphenol A (BPA), an environmental estrogen, is widely used and largely released into the hydrosphere, thus inducing adverse effects in aquatic organisms. Here, Xenopus tropicalis was used as an animal model to investigate the oxidative effects of BPA on early embryonic development. BPA exposure prevalently caused development delay and shortened body length. Furthermore, BPA exposure significantly increased the levels of reactive oxygen species (ROS) and DNA damage in embryos. Thus, the details of BPA interference with antioxidant regulatory pathways during frog early embryonic development should be further explored.