Enhanced heterozygosity from male meiotic chromosome chains is superseded by hybrid female asexuality in termites

2021 ◽  
Vol 118 (51) ◽  
pp. e2009533118
Author(s):  
Toshihisa Yashiro ◽  
Yi-Kai Tea ◽  
Cara Van Der Wal ◽  
Tomonari Nozaki ◽  
Nobuaki Mizumoto ◽  
...  

Although males are a ubiquitous feature of animals, they have been lost repeatedly in diverse lineages. The tendency for obligate asexuality to evolve is thought to be reduced in animals whose males play a critical role beyond the contribution of gametes, for example, via care of offspring or provision of nuptial gifts. To our knowledge, the evolution of obligate asexuality in such species is unknown. In some species that undergo frequent inbreeding, males are hypothesized to play a key role in maintaining genetic heterozygosity through the possession of neo-sex chromosomes, although empirical evidence for this is lacking. Because inbreeding is a key feature of the life cycle of termites, we investigated the potential role of males in promoting heterozygosity within populations through karyotyping and genome-wide single-nucleotide polymorphism analyses of the drywood termite Glyptotermes nakajimai. We showed that males possess up to 15 out of 17 of their chromosomes as sex-linked (sex and neo-sex) chromosomes and that they maintain significantly higher levels of heterozygosity than do females. Furthermore, we showed that two obligately asexual lineages of this species—representing the only known all-female termite populations—arose independently via intraspecific hybridization between sexual lineages with differing diploid chromosome numbers. Importantly, these asexual females have markedly higher heterozygosity than their conspecific males and appear to have replaced the sexual lineages in some populations. Our results indicate that asexuality has enabled females to supplant a key role of males.

2010 ◽  
Vol 70 (4) ◽  
pp. 668-674 ◽  
Author(s):  
P Dieudé ◽  
M Guedj ◽  
J Wipff ◽  
B Ruiz ◽  
G Riemekasten ◽  
...  

BackgroundRecent evidence has highlighted a potential role of interleukin 1β (IL-1β) in systemic sclerosis (SSc). NLRP1 provides a scaffold for the assembly of the inflammasome that promotes the processing and maturation of pro-IL-1β. In addition, NLRP1 variants were found to confer susceptibility to autoimmune disorders.ObjectiveTo study a possible association of the NLRP1 rs6502867, rs2670660 and rs8182352, rs12150220 and rs4790797 with SSc in the European Caucasian population.MethodsNLRP1 single nucleotide polymorphisms were genotyped in 3227 individuals comprising a discovery set (870 SSc patients and 962 controls) and a replication set including individuals from Germany (532 SSc patients and 324 controls) and Italy (527 SSc patients and 301 controls), all individuals being of European Caucasian origin.ResultsConditional analyses revealed a significant association for the NLRP1 rs8182352 variant with both anti-topoisomerase-positive and SSc-related fibrosing alveolitis (FA) subsets under an additive model: p=0.0042, OR 1.23 (95% CI 1.07 to 1.41) and p=0.0065 OR 1.19 (95% CI 1.05 to 1.36), respectively. Logistic regression analysis showed an additive effect of IRF5 rs2004640, STAT4 rs7574865 and NLRP1 rs8182352 risk alleles on SSc-related FA.ConclusionsOur results establish NLRP1 as a new genetic susceptibility factor for SSc-related pulmonary fibrosis and anti-topoisomerase-positive SSc phenotypes. This provides new insights into the pathogenesis of SSc, underlining the potential role of innate immunity in particular in the FA-positive SSc subphenotype, which represents a severe subset of the disease.


2011 ◽  
Vol 96 (2) ◽  
pp. E394-E403 ◽  
Author(s):  
Neeraj K. Sharma ◽  
Kurt A. Langberg ◽  
Ashis K. Mondal ◽  
Steven C. Elbein ◽  
Swapan K. Das

abstract Context: Genome-wide association scans (GWAS) have identified novel single nucleotide polymorphisms (SNPs) that increase T2D susceptibility and indicated the role of nearby genes in T2D pathogenesis. Objective: We hypothesized that T2D-associated SNPs act as cis-regulators of nearby genes in human tissues and that expression of these transcripts may correlate with metabolic traits, including insulin sensitivity (SI). Design, Settings, and Patients: Association of SNPs with the expression of their nearest transcripts was tested in adipose and muscle from 168 healthy individuals who spanned a broad range of SI and body mass index (BMI) and in transformed lymphocytes (TLs). We tested correlations between the expression of these transcripts in adipose and muscle with metabolic traits. Utilizing allelic expression imbalance (AEI) analysis we examined the presence of other cis-regulators for those transcripts in TLs. Results: SNP rs9472138 was significantly (P = 0.037) associated with the expression of VEGFA in TLs while rs6698181 was detected as a cis-regulator for the PKN2 in muscle (P = 0.00027) and adipose (P = 0.018). Significant association was also observed for rs17036101 (P = 0.001) with expression of SYN2 in adipose of Caucasians. Among 19 GWAS-implicated transcripts, expression of VEGFA in adipose was correlated with BMI (r = −0.305) and SI (r = 0.230). Although only a minority of the T2D-associated SNPs were validated as cis-eQTLs for nearby transcripts, AEI analysis indicated presence of other cis-regulatory polymorphisms in 54% of these transcripts. Conclusions: Our study suggests that a small subset of GWAS-identified SNPs may increase T2D susceptibility by modulating expression of nearby transcripts in adipose or muscle.


Author(s):  
Yunkai Zhu ◽  
Fei Feng ◽  
Gaowei Hu ◽  
Yuyan Wang ◽  
Yin Yu ◽  
...  

SUMMARYThe global spread of SARS-CoV-2 is posing major public health challenges. One unique feature of SARS-CoV-2 spike protein is the insertion of multi-basic residues at the S1/S2 subunit cleavage site, the function of which remains uncertain. We found that the virus with intact spike (Sfull) preferentially enters cells via fusion at the plasma membrane, whereas a clone (Sdel) with deletion disrupting the multi-basic S1/S2 site instead utilizes a less efficient endosomal entry pathway. This idea was supported by the identification of a suite of endosomal entry factors specific to Sdel virus by a genome-wide CRISPR-Cas9 screen. A panel of host factors regulating the surface expression of ACE2 was identified for both viruses. Using a hamster model, animal-to-animal transmission with the Sdel virus was almost completely abrogated, unlike with Sfull. These findings highlight the critical role of the S1/S2 boundary of the SARS-CoV-2 spike protein in modulating virus entry and transmission.


2021 ◽  
Vol 12 ◽  
Author(s):  
Siqi Ming ◽  
Mei Zhang ◽  
Zibin Liang ◽  
Chunna Li ◽  
Jianzhong He ◽  
...  

Mucosal associated invariant T (MAIT) cells play a critical role in Helicobacter pylori (H. pylori)-induced gastritis by promoting mucosal inflammation and aggravating mucosal injuries (1, 2). However, the underlying mechanism and key molecules involved are still uncertain. Here we identified OX40, a co-stimulatory molecule mainly expressed on T cells, as a critical regulator to promote proliferation and IL-9 production by MAIT cells and facilitate mucosal inflammation in H. pylori-positive gastritis patients. Serum examination revealed an increased level of IL-9 in gastritis patients. Meanwhile, OX40 expression was increased in mucosal MAIT cells, and its ligand OX40L was also up-regulated in mucosal dendritic cells (DCs) of gastritis patients, compared with healthy controls. Further results demonstrated that activation of the OX40/OX40L pathway promoted IL-9 production by MAIT cells, and MAIT cells displayed a highly-activated phenotype after the cross-linking of OX40 and OX40L. Moreover, the level of IL-9 produced by MAIT cells was positively correlated with inflammatory indexes in the gastric mucosa, suggesting the potential role of IL-9-producing MAIT cells in mucosal inflammation. Taken together, we elucidated that OX40/OX40L axis promoted mucosal MAIT cell proliferation and IL-9 production in H. pylori-induced gastritis, which may provide potential targeting strategies for gastritis treatment.


2020 ◽  
Author(s):  
Divya Kattupalli ◽  
Asha Sriniva ◽  
Soniya E V

Abstract Background: Black pepper is a prominent spice which is an indispensable ingredient in culinary and traditional medicine. Phytophthora capsici, the causative agent of foot rot disease causes drastic constraint in black pepper cultivation and productivity. To counterattack various biotic and abiotic stresses plants employ a broad array of mechanisms one such includes the accumulation of pathogenesis-related (PR) proteins. Several studies have reported the role of PR-1 proteins in triggering the plant defenses during plant-oomycete interaction.Results: Through the genome-wide survey, eleven PR-1 genes that belongs to a CAP superfamily protein with Caveolin-Binding Motif (CBM) and CAP-derived peptide (CAPE) were identified from P. nigrum. Despite the critical functional domains, PnPR1 homologs differ in their signal peptide motifs, and core amino acid sequence composition in the functional protein domains. The GO, biological function analysis reveals their role in defense responses and response to biotic stimulus whereas the KEGG functional annotation predicted their function in the plant-pathogen interactions. Furthermore, transcriptome-assisted FPKM analysis revealed PnPR-1 genes mapped to P. nigrum - P. capsici interaction pathway. The differentially expressed pathogen-responsive PR-1 gene was validated through qRT-PCR. Subsequent analysis revealed the structural details, phylogenetic relationships, conserved sequence motifs and critical cis-regulatory elements of PnPR-1 genes.Conclusion: This is the first genome-wide study that identified the role of PR-1 genes during P. nigrum - P. capsici interactions. The detailed in silico experimental analysis revealed the vital role of PnPR-1 genes in regulating the first layer of defense towards P. capsici infection in Panniyur-1 plants.


2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Jing Shen ◽  
Shuang Wang ◽  
Abby B. Siegel ◽  
Helen Remotti ◽  
Qiao Wang ◽  
...  

Background.Previous studies, including ours, have examined the regulation of microRNAs (miRNAs) by DNA methylation, but whether this regulation occurs at a genome-wide level in hepatocellular carcinoma (HCC) is unclear.Subjects/Methods.Using a two-phase study design, we conducted genome-wide screening for DNA methylation and miRNA expression to explore the potential role of methylation alterations in miRNAs regulation.Results.We found that expressions of 25 miRNAs were statistically significantly different between tumor and nontumor tissues and perfectly differentiated HCC tumor from nontumor. Six miRNAs were overexpressed, and 19 were repressed in tumors. Among 133 miRNAs with inverse correlations between methylation and expression, 8 miRNAs (6%) showed statistically significant differences in expression between tumor and nontumor tissues. Six miRNAs were validated in 56 additional paired HCC tissues, and significant inverse correlations were observed for miR-125b and miR-199a, which is consistent with the inactive chromatin pattern found in HepG2 cells.Conclusion.These data suggest that the expressions of miR-125b and miR-199a are dramatically regulated by DNA hypermethylation that plays a key role in hepatocarcinogenesis.


The Healer ◽  
2021 ◽  
Vol 2 (1) ◽  
pp. 80-86
Author(s):  
Shankar Gautam ◽  
Abhishek Upadhyay ◽  
Rashmi Mutha ◽  
BINOD KUMAR SINGH ◽  
Ram Kishor Joshi

Diabetes is a clinical condition characterized by a spike in blood glucose in plasma. It is one of the 21st century's greatest public health crises and is among the top 10 causes of death worldwide. Although new drugs and therapeutics are emerging for its management but the prevalence is increasing at an alarming pace; thus, every system must contribute for effective management. An effort is made to review the efficacy and safety evaluation of the individual herbs of Darvyadi Kwatha (DK), an Ayurvedic formulation mentioned in Charaka Samhita. The constituents of the DK has some strong efficient antidiabetic/hypoglycaemic chemical principle having insulin-triggering and insulin-like behaviors which increases the activity of glucose-6-phosphate dehydrogenase (G6PD) and glucokinase and decreases glucose-6-phosphatase activity, reduce oxidative stress and prevention of glutathione reductase, superoxide dismutase, and catalase activity play a critical role in glucose homeostasis. DK also improve biochemical parameters such as SGPT, SGOT, cholesterol and triglycerides and is found to be safe in animal experiments. The various evidences clearly indicates that DK has definite hypoglycemic potential as well as anti-diabetic activity.


Sports ◽  
2018 ◽  
Vol 6 (3) ◽  
pp. 88 ◽  
Author(s):  
Ysabel Jacob ◽  
Tania Spiteri ◽  
Nicolas Hart ◽  
Ryan Anderton

In elite sporting codes, the identification and promotion of future athletes into specialised talent pathways is heavily reliant upon objective physical, technical, and tactical characteristics, in addition to subjective coach assessments. Despite the availability of a plethora of assessments, the dependence on subjective forms of identification remain commonplace in most sporting codes. More recently, genetic markers, including several single nucleotide polymorphisms (SNPs), have been correlated with enhanced aerobic capacity, strength, and an overall increase in athletic ability. In this review, we discuss the effects of a number of candidate genes on athletic performance, across single-skilled and multifaceted sporting codes, and propose additional markers for the identification of motor skill acquisition and learning. While displaying some inconsistencies, both the ACE and ACTN3 polymorphisms appear to be more prevalent in strength and endurance sporting teams, and have been found to correlate to physical assessments. More recently, a number of polymorphisms reportedly correlating to athlete performance have gained attention, however inconsistent research design and varying sports make it difficult to ascertain the relevance to the wider sporting population. In elucidating the role of genetic markers in athleticism, existing talent identification protocols may significantly improve—and ultimately enable—targeted resourcing in junior talent pathways.


2018 ◽  
Author(s):  
Rakesh Pathak ◽  
Priyanka Singh ◽  
Sudha Ananthakrishnan ◽  
Sarah Adamczyk ◽  
Olivia Schimmel ◽  
...  

ABSTRACTHistone chaperones, chromatin remodelers, and histone modifying complexes play a critical role in alleviating the nucleosomal barrier. Here, we have examined the role of two highly conserved yeast (Saccharomyces cerevisiae) histone chaperones, FACT and Spt6, in regulating transcription and histone occupancy. We show that the H3 tail contributes to the recruitment of FACT to coding sequences in a manner dependent on acetylation. We found that deleting a H3 HAT Gcn5 or mutating lysines on the H3 tail impairs FACT recruitment at ADH1 and ARG1 genes. However, deleting the H4 tail or mutating the H4 lysines failed to dampen FACT occupancy in coding regions. Additionally, we show that FACT-depletion greatly reduces Pol II occupancy in the 5’ ends genome-wide. By contrast, Spt6-depletion led to reduction in Pol II occupancy towards the 3’ end, in a manner dependent on the gene-length. Severe transcription and histone eviction defects were also observed in a strain that was impaired for Spt6 recruitment (spt6Δ202) and depleted of FACT. Importantly, the severity of the defect strongly correlated with WT Pol II occupancies at these genes, indicating critical roles of Spt6 and Spt16 in promoting high-level transcription. Collectively, our study shows cooperation, as well as redundancy between chaperones, FACT and Spt6, in regulating transcription and chromatin in coding regions of transcribed genes.


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