Biology subjects

Wang, R. W.

Publications and source records attributed to Wang, R. W..

4 recordsLinked to original sources

bioRxiv2022

CHDbase: A Comprehensive Knowledgebase for Congenital Heart Disease-related Genes and Clinical Manifestations

Congenital heart disease (CHD) is the most common cause of major birth defects, with a prevalence of 1%. Although an increasing number of studies reporting the etiology of CHD, the findings scattered throughout the literature are difficult to retrieve and utilize in research and clinical practice. We therefore developed CHDbase, an evidence-based knowledgebase with CHD-related genes and clinical manifestations manually curated from 1114 publications, linking 1124 susceptibility genes and 3591 variations to more than 300 CHD types and related syndromes. Metadata such as the information of each publication and the selected population and samples, the strategy of studies, and the major findings of study were integrated with each item of research record. We also integrated functional annotations through parsing ~50 databases/tools to facilitate the interpretation of these genes and variations in disease pathogenicity. We further prioritized the significance of these CHD-related genes with a gene interaction network approach, and extracted a core CHD sub-network with 163 genes. The clear genetic landscape of CHD enables the phenotype classification based on the shared genetic origin. Overall, CHDbase provides a comprehensive and freely available resource to study CHD susceptibility, supporting a wide range of users in the scientific and medical communities. CHDbase is accessible at http://chddb.fwgenetics.org/.

genetics↗

bioRxiv2020

Aneuploid cells activate NF-κB to promote their immune clearance by NK cells

SummaryThe immune system plays a major role in the protection against cancer. Identifying and characterizing the pathways mediating this immune surveillance is thus critical for understanding how cancer cells are recognized and eliminated. We previously found that untransformed cells that had undergone senescence due to highly abnormal karyotypes are eliminated by Natural Killer (NK) cells in vitro. Here we show that this is also true for aneuploid untransformed cells that had not lost their ability to proliferate. Their elimination by NK cells, like that of aneuploid senescent cells, is predominantly mediated by non-cell autonomous mechanisms. Our data further indicate that NF-κB signaling in aneuploid cells is central to eliciting this immune response. Inactivating NF-κB abolishes NK-cell mediated clearance in aneuploid cells in vitro. In cancer cell lines, NF-κB signaling correlates with degree of aneuploidy, raising the possibility that aneuploidy-induced immune recognition is partially retained in cancer.Competing Interest StatementThe authors have declared no competing interest.View Full Text

cancer biology↗

bioRxiv2020

Weak predation strength promotes stable coexistence of predators and prey in the same chain and across chains

The mechanisms of species coexistence make ecologists fascinated, although theoretical work show that omnivory can promote coexistence of species and food web stability, it is still a lack of the general mechanisms for species coexistence in the real food webs, and is unknown how omnivory affects the interactions between competitor and predator. In this work, we first establish an omnivorous food web model with a competitor based on two natural ecosystems (the plankton community and fig-fig wasp system). We analyze the changes of both food web structure and stability under the different resource levels and predation preference of the generalist/top predator. The results of model analyses show that weak predation strength can promote stable coexistence of predators and prey. Moreover, evolutionary trend of food web structure changes with the relative predation strength is more diversity than the relative competition strength, and an integration of both omnivory, increased competition, top-down control and bottom-up control can promote species diversity and food web stability. Our theoretical predictions are consistent with empirical data in the plankton community: the lower concentration of nutrient results in a more stable population dynamics. Our theoretical work could enrich the general omnivorous theory on species coexistence and system stability in the real food webs.

ecology↗

bioRxiv2017

Position Effects Influencing Intrachromosomal Repair of a Double-Strand Break in Budding Yeast

Repair of a double-strand break (DSB) by an ectopic homologous donor sequence is subject to the three-dimensional arrangement of chromosomes in the nucleus of haploid budding yeast. The data for interchromosomal recombination suggest that searching for homology is accomplished by a random collision process, strongly influenced by the contact probability of the donor and recipient sequences. Here we explore how recombination occurs on the same chromosome and whether there are additional constraints imposed on repair. Specifically, we examined how intrachromosomal repair is affected by the location of the donor sequence along the 812-kb chromosome 2 (Chr2), with a site-specific DSB created on the right arm (position 625kb). Repair correlates well with contact frequencies determined by chromosome conformation capture-based studies (r = 0.85). Moreover, there is a profound constraint imposed by the anchoring of the centromere (CEN2, position 238kb) to the spindle pole body. Sequences at the same distance on either side of CEN2 are equivalently constrained in recombining with a DSB located more distally on one arm, suggesting that sequences on the opposite arm from the DSB are not otherwise constrained in their interaction with the DSB. The centromere constraint can be partially relieved by inducing transcription through the centromere to inactivate CEN2 tethering. In diploid cells, repair of a DSB via its allelic donor is strongly influenced by the presence and the position of an ectopic intrachromosomal donor.\n\nAuthor SummaryA double-strand break (DSB) on a chromosome can be repaired by recombining with an ectopic homologous donor sequence. Interchromosomal ectopic recombination is strongly influenced by the three-dimensional arrangement of chromosomes in the nucleus of haploid budding yeast, that is strongly influenced by the probability of chemical cross-linking of the donor and recipient sequences. Here we explore how recombination occurs on the same chromosome. We examined how intrachromosomal repair is affected by the location of the donor sequence along the 812-kb chromosome 2 (Chr2), with a site-specific DSB created on the right arm (position 625kb). Repair correlates well with contact frequencies determined by chromosome conformation capture-based studies (r = 0.85). Moreover, there is a profound constraint imposed by the anchoring of the centromere (CEN2, position 238kb) to the spindle pole body. Sequences at the same distance on either side of CEN2 are equivalently accessible in recombining with a DSB located more distally on one arm, suggesting that sequences on the opposite arm from the DSB are not otherwise constrained in their interaction with the DSB. The centromere constraint can be partially relieved by inducing transcription through the centromere to inactivate CEN2 tethering. In diploid cells, repair of a DSB via its allelic donor is strongly influenced by the presence and the position of an ectopic intrachromosomal donor.

genetics↗