Genetic differentiation and phylogeography of rotifer Polyarthra dolichoptera and P. vulgaris populations between Southeastern China and eastern North America: High intercontinental differences

Genetic differentiations and phylogeographical patterns of small organisms may be shaped by spatial isolation, environmental gradients, and gene flow. However, knowledge about genetic differentiation of rotifers at the intercontinental scale is still limited. Polyarthra dolichoptera and P. vulgaris are cosmopolitan rotifers that are tolerant to environmental changes, offering an excellent model to address the research gap. Here, we investigated the populations in Southeastern China and eastern North America and evaluated the phylogeographical patterns from their geographical range sizes, geographic–genetic distance relationships and their responses to spatial‐environmental factors. Using the mitochondrial cytochrome c oxidase subunit I gene as the DNA marker, we analyzed a total of 170 individuals. Our results showed that some putative cryptic species, also known as entities were widely distributed, but most of them were limited to single areas. The divergence of P. dolichoptera and P. vulgaris indicated that gene flow between continents was limited while that within each continent was stronger. Oceanographic barriers do affect the phylogeographic pattern of rotifers in continental waters and serve to maintain genetic diversity in nature. The genetic distance of P. dolichoptera and P. vulgaris populations showed significant positive correlation with geographic distance. This might be due to the combined effects of habitat heterogeneity, long‐distance colonization, and oceanographic barriers. Furthermore, at the intercontinental scale, spatial distance had a stronger influence than environmental variables on the genetic differentiations of both populations. Wind‐ and animal‐mediated transport and even historical events of continental plate tectonics are potential factors for phylogeography of cosmopolitan rotifers.     

A Fast EM Algorithm for BayesA-Like Prediction of Genomic Breeding Values

Prediction accuracies of estimated breeding values for economically important traits are expected to benefit from genomic information. Single nucleotide polymorphism (SNP) panels used in genomic prediction are increasing in density, but the Markov Chain Monte Carlo (MCMC) estimation of SNP effects can be quite time consuming or slow to converge when a large number of SNPs are fitted simultaneously in a linear mixed model. Here we present an EM algorithm (termed “fastBayesA”) without MCMC. This fastBayesA approach treats the variances of SNP effects as missing data and uses a joint posterior mode of effects compared to the commonly used BayesA which bases predictions on posterior means of effects. In each EM iteration, SNP effects are predicted as a linear combination of best linear unbiased predictions of breeding values from a mixed linear animal model that incorporates a weighted marker-based realized relationship matrix. Method fastBayesA converges after a few iterations to a joint posterior mode of SNP effects under the BayesA model. When applied to simulated quantitative traits with a range of genetic architectures, fastBayesA is shown to predict GEBV as accurately as BayesA but with less computing effort per SNP than BayesA. Method fastBayesA can be used as a computationally efficient substitute for BayesA, especially when an increasing number of markers bring unreasonable computational burden or slow convergence to MCMC approaches.     

Crossregulation of beta-catenin/Tcf pathway by NF-kappaB is mediated by lzts2 in human adipose tissue-derived mesenchymal stem cells

beta-catenin/Tcf and NF-kappaB signaling pathways play an important role in biological functions and crosstalk between these pathways has been reported. We found that the modulation of NF-kappaB activity showed a direct correlation with beta-catein/Tcf pathway in human adipose tissue (hASCs) and bone marrow (hBMSCs)-derived mesenchymal stem cells. Expression of lzts2, which inhibits nuclear translocation of beta-catenin and its transactivation activity, was regulated by NF-kappaB activity. Downregulation of lzts2 by RNA interference increased the nuclear translocation of beta-catenin and NF-kappaB activity in hASCs. NF-kappaB activation by the downregulation of lzts2 was accompanied by the increase of beta-TrCP1 expression and the decrease of IkappaB level. Downregulation of lzts2 increased the proliferation of hASCs and hBMSC, and blocked the NF-kappaB inhibitor-induced inhibitory effect on their proliferation and Tcf promoter activation. These findings provide the first evidence that the reciprocal crosstalk between beta-catenin/Tcf pathway and NF-kappaB signaling in hMSCs is mediated through the regulation of lzts2 expression.     

Deciphering the SUMO code in the kidney

SUMOylation of proteins is an important regulatory element in modulating protein function and has been implicated in the pathogenesis of numerous human diseases such as cancers, neurodegenerative diseases, brain injuries, diabetes, and familial dilated cardiomyopathy. Growing evidence has pointed to a significant role of SUMO in kidney diseases such as DN, RCC, nephritis, AKI, hypertonic stress and nephrolithiasis. Recently, emerging studies in podocytes demonstrated that SUMO might have a protective role against podocyte apoptosis. However, the SUMO code responsible for beneficial outcome in the kidney remains to be decrypted. Our recent experiments have revealed that the expression of both SUMO and SUMOylated proteins is appreciably elevated in hypoxia‐induced tubular epithelial cells (TECs) as well as in the unilateral ureteric obstruction (UUO) mouse model, suggesting a role of SUMO in TECs injury and renal fibrosis. In this review, we attempt to decipher the SUMO code in the development of kidney diseases by summarizing the defined function of SUMO and looking forward to the potential role of SUMO in kidney diseases, especially in the pathology of renal fibrosis and CKD, with the goal of developing strategies that maximize correct interpretation in clinical therapy and prognosis.     

Variation of phenotype,ploidy level,and organogenic potential of in vitro regenerated polyploids of <Emphasis Type=Italic>Pyrus communis</Emphasis>

A wide range of phenotypic variation was observed among neopolyploids obtained from the diploid pear cultivar ‘Fertility’ by in vitro colchicine treatment. The variant plantlets had alterations in leaf characteristics. Neopolyploids had significantly different ratios of leaf length to leaf width compared to the diploid control. Shoot regeneration from leaf explants and rooting ability from in vitro shoots of neopolyploids was examined. Regeneration frequencies of shoots from leaf explants of seven of the nine neopolyploids were significantly decreased compared to the diploid control. The organogenic potential of neopolyploids was highly genotype-dependent for both shoots and roots. Tetraploid clone 4x − 4 failed to regenerate shoots from leaf explants and the pentaploid clone 5x − 2 failed to root from in vitro shoots. The results suggest that polyploidization caused the decrease in or loss of in vitro organogenic potential. Regenerated shoots derived from neopolyploids showed different phenotypes, depending on the ploidy of the donor plant.     

A novel 62‐bp indel mutation in the promoter region of transforming growth factor‐beta 2 (TGFB2) gene is associated with body weight in chickens

Transforming growth factor‐beta 2 (encoded by TGFB2) is a growth factor that regulates a plethora of cellular functions. In this study, we sequenced the promoter and full‐length exon region of the chicken TGFB2 and found two mutations (g.‐640C>T and g.‐851_‐790del) within the promoter. The two polymorphisms were genotyped in 1030 pedigreed hens recorded for body weight at 7 (BW7), 9 (BW9), 11 (BW11), 13 (BW13), 17 (BW17) weeks old, egg weight at 36 weeks of age (EW36) and egg numbers from the age at first egg (AFE) to 40 weeks of age (EN40). Despite the fact that no mutations were found to have statistically significant genetic effects on egg production, the association results of growth traits showed that both g.‐640C>T and g.‐851_‐790del had significant effects on body weights and that both genotype g.‐640TT and g.‐851_‐790wt/wt were positive for body weight performance. Therefore, the polymorphisms of TGFB2, especially the g.‐851_‐790del mutation associated with body weight at almost all periods, could be potential useful genetic markers to improve the growth of Beijing You chickens.