Biology subjects

Chai, W.

Publications and source records attributed to Chai, W..

2 recordsLinked to original sources

bioRxiv2019

Genome-wide mapping and profiling of γH2AX binding hotspots in response to different replication stress inducers

BackgroundReplication stress (RS) gives rise to DNA damage that threatens genome stability. RS can originate from different sources that stall replication by diverse mechanisms. However, the mechanism underlying how different types of RS contribute to genome instability is unclear, in part due to the poor understanding of the distribution and characteristics of damage sites induced by different RS mechanisms.\n\nResultsWe use ChIP-seq to map {gamma}H2AX binding sites genome-wide caused by aphidicolin (APH), hydroxyurea (HU), and methyl methanesulfonate (MMS) treatments in human lymphocyte cells. Mapping of {gamma}H2AX ChIP-seq reveals that APH, HU, and MMS treatments induce non-random {gamma}H2AX chromatin binding at discrete regions, suggesting that there are {gamma}H2AX binding hotspots in the genome. Characterization of the distribution and sequence/epigenetic features of {gamma}H2AX binding sites reveals that the three treatments induce {gamma}H2AX binding at largely non-overlapping regions, suggesting that RS may cause damage at specific genomic loci in a manner dependent on the fork stalling mechanism. Nonetheless, {gamma}H2AX binding sites induced by the three treatments share common features including compact chromatin, coinciding with larger-than-average genes, and depletion of CpG islands and transcription start sites. Moreover, we observe significant enrichment of SINEs in {gamma}H2AX sites in all treatments, indicating that SINEs may be a common barrier for replication polymerases.\n\nConclusionsOur results identify the location and common features of genome instability hotspots induced by different types of RS, and help in deciphering the mechanisms underlying RS-induced genetic diseases and carcinogenesis.

genomics↗

bioRxiv2018

Quantum energy levels of glutamate modulate neural biophotonic signals

Glutamate is the most abundant excitatory neurotransmitter in the brain, and it plays an essential and important role in neural functions. Hypofunction of the glutamatergic pathway and the changes in the glutamate-glutamine cycle function are important neuropathological mechanisms of severe mental disorders including schizophrenia and depression. Current studies have shown that glutamate can induce neural biophotonic activity and transmission, which may involve the mechanism of photon quantum brain; however, it is unclear whether such a mechanism follows the principle of quantum mechanics. Here we show that the action of glutamate on its receptors leads to a decrease in its quantum energy levels, and glutamate then partially or completely loses its function to further induce the biophotonic activity in mouse brain slices. The reduced quantum energy levels of glutamate can be restored by direct-current electrical discharges and the use of energy transfer of chloroplast photosynthesis; hence, the quantum energy recovered glutamate can again induce significant biophotonic activity. Furthermore, the changes in quantum energy levels of glutamate are related to the exchange and transfer of electron energy on its active hydrogen atom. These findings suggest that the glutamate-induced neural biophotonic signals may be involved in the transfer of the quantum energy levels of glutamate, which implies a quantum mechanism of neurotransmitter action. The process of glutamate recycling that is related to the synergism of neurons and glial cells and certain key enzymes may be necessary for the recovery of quantum energy levels of glutamate after completion of the neural signal transmission. These findings may also provide a new idea to develop \"quantum drugs\".

neuroscience↗