Estimation of variance components for carcass traits in Japanese Black cattle using 50K SNP genotype data

Genomic selection using high‐density single nucleotide polymorphism (SNP) genotype data may accelerate genetic improvements in livestock animals. In this study, we attempted to estimate the variance components of six carcass traits in fattened Japanese Black steers using SNP genotype data. Six hundred and seventy‐three steers were genotyped using an Illumina Bovine SNP50 BeadChip and phenotyped for cold carcass weight, ribeye area, rib thickness, subcutaneous fat thickness, estimated yield percent and marbling score. Additive polygenic variance and the variance attributable to a set of SNPs that had statistically significant effects on the trait were estimated via Gibbs sampling with two models: (i) a model with the chosen SNPs and the additive polygenic effects; and (ii) a model with the polygenic effects alone. The proportion of the estimated variance attributable to the SNPs became higher as the number of SNP effects that fit increased. High correlations between breeding values estimated with the model containing the polygenic effect alone and those estimated by chosen SNPs were obtained. No fraction of the total genetic variance was explained by SNPs associated with the trait at P ≥ 0.1. Our results suggest that for the carcass traits of Japanese Black cattle, a maximum of half of the total additive genetic variance may be explained by SNPs between 100 several tens to several 100s.     

Hepatic gene expression of the insulin signaling pathway is altered by administration of persimmon peel extract: a DNA microarray study using type 2 diabetic Goto-Kakizaki rats

Persimmon (Diospyros kaki) is a very popular fruit in East Asian countries, but its peels are not consumed despite the fact that they contain many antioxidants such as carotenoids and polyphenols. We prepared a fat-soluble extract from persimmon peel (PP) and fed type 2 diabetic Goto-Kakizaki (GK) rats an AIN-93G rodent diet supplemented with persimmon peel extract (PP diet) for 12 weeks. Compared with the control AIN-93G diet, the PP diet significantly reduced plasma glutamic-pyruvate transaminase activity, with accumulation of β-cryptoxanthin in the liver. DNA microarray analysis revealed that the PP diet altered hepatic gene expression profiles. In particular, expression of insulin signaling pathway-related genes was significantly enriched in differentially expressed gene sets. Moreover, Western blotting analysis showed an increase in insulin receptor beta tyrosine phosphorylation in rats fed the PP diet. These data suggest that the PP diet improves insulin resistance in GK rats.     

An expanded palette of genetically encoded Ca²⁺ indicators

Engineered fluorescent protein (FP) chimeras that modulate their fluorescence in response to changes in calcium ion (Ca(2+)) concentration are powerful tools for visualizing intracellular signaling activity. However, despite a decade of availability, the palette of single FP-based Ca(2+) indicators has remained limited to a single green hue. We have expanded this palette by developing blue, improved green, and red intensiometric indicators, as well as an emission ratiometric indicator with an 11,000% ratio change. This series enables improved single-color Ca(2+) imaging in neurons and transgenic Caenorhabditis elegans. In HeLa cells, Ca(2+) was imaged in three subcellular compartments, and, in conjunction with a cyan FP-yellow FP-based indicator, Ca(2+) and adenosine 5'-triphosphate were simultaneously imaged. This palette of indicators paints the way to a colorful new era of Ca(2+) imaging.     

Kidney organoid derived from renal tissue stem cells is a useful tool for histopathological assessment of nephrotoxicity in a cisplatin-induced acute renal tubular injury model

Organoids derived from renal tissue stem cells (KS cells) isolated from the S3 segment of adult rat nephrons have previously been developed and evaluated. However, data regarding the histopathological evaluation of these organoids are limited. Therefore, in this study, we performed histopathological examinations of the properties of these organoids and evaluated the nephrotoxicity changes induced by cisplatin treatment. We observe that the tubular structure of the organoids was generally lined by a single layer of cells, in concordance with previous findings. Microvilli were exclusively observed under electron microscopy on the luminal side of this tubular structure. Moreover, the luminal side of the tubular structure was positive for aquaporin-1 (Aqp1), a marker of the proximal renal tubule. Cisplatin treatment induced cell death and degeneration, including cytoplasmic vacuolation, in cells within the tubular structure of the organoids. Cisplatin toxicity is associated with the induction of γ-H2AX (a marker of DNA damage) and the drop of phospho-histone H3 (a marker of cell division) levels. During the nephrotoxicity assessment, the kidney organoids displayed various features similar to those of the natural kidney, suggesting that it is possible to use these organoids in predicting nephrotoxicity. The histological evaluation of the organoids in this study provides insights into the mechanisms underlying nephrotoxicity.     

Population structure of Nga Myin Yinn Silonia silondia in the Ayeyarwady River,Myanmar, by mitochondrial DNA markers

Fisheries Science - The Silond catfish Silonia silondia, locally known as Nga Myin Yinn, is a commercially important fish in Myanmar; however, fundamental knowledge of its population structure is...     

The Colletotrichum higginsianum secreted effector protein ChEC91 induces plant cell death

ChEC91, a novel cell death-inducing effector protein from the fungal pathogen Colletotrichum higginsianum, causal agent of crucifer anthracnose disease, is described. Both transient expression of ChEC91 and infiltration of purified recombinant protein induced necrotic lesions in Nicotiana benthamiana leaves. The recombinant protein also induced electrolyte leakage and callose deposition in Arabidopsis thaliana leaf tissue and the expression of defence marker genes. Moreover, fungal mutants constitutively over-expressing ChEC91 in C. higginsianum were impaired in appressorial penetration on Brassica rapa cotyledons. These results suggest that inappropriate expression of ChEC91 might negatively affect the early stage of C. higginsianum infection by inducing plant defence responses. Protein domain deletion analysis showed that the C-terminal region of ChEC91 was necessary, but not sufficient, for activity in N. benthamiana. Homologous effector proteins cloned from C. gloeosporioides, Fusarium graminearum, and Pyricularia oryzae differed in their cell death-inducing activity, which appeared related to sequence variations in the C-terminal region of these proteins. Moreover, this region contained amino acid residues that were well conserved within Colletotrichum species. These results suggest that the amino acid residues in the C-terminal region may be important for inducing cell death in plants.

     

Magnetic resonance imaging assessment of pituitary posterior lobe displacement in dogs with pituitary-dependent hyperadrenocorticism

The displacement and signal intensity (SI) of the pituitary posterior lobe were evaluated on T1 weighted magnetic resonance (MR) images in 28 dogs with pituitary dependent hyperadrenocorticism (PDH). Compared with normal dogs, the posterior lobe was displaced dorsally in the pituitary of the PDH dogs. Correlation between the pituitary height/brain area (P/B) ratio and the displacement of the posterior lobe in the PDH dogs suggests that dorsal displacement of the posterior lobe increases in accordance with enlargement of the pituitary. As to the SI of the posterior lobe, the PDH dogs showed significantly lower SI in comparison to the normal dogs. Taken together, these results suggest that assessment of the displacement and SI of the posterior lobe of the pituitary on T1-weighted MR images is useful for the diagnosis of pituitary adenoma. In pituitary microadenoma that presents no apparent tumorigenesis on MRI, evaluation of these values may be useful for diagnosis and selection of an appropriate therapy.     

Production of lipid mediators in mastitic milk of cow

Bovine mastitis is one of the most prevalent and costly diseases in the dairy industry. Lipid mediators are signaling molecules which coordinately and intricately modulate inflammation. They are produced from polyunsaturated fatty acids (PUFAs) in the cellular membrane via several enzymes including cyclooxygenase (COX) and lipoxygenase (LOX). In the present study, we performed comprehensive analysis of lipid production in milk obtained from clinical or subclinical mastitic cows using liquid chromatography/mass spectrometry. We detected 26, 24, and 40 kinds of lipid constantly in healthy, subclinical, and clinical mastitic milk, respectively. In clinical mastitic milk, the amount of a major n‐6 PUFA, arachidonic acid (AA), tended to increase, whereas amounts of major n‐3 PUFAs, eicosapentaenoic acid and docosahexaenoic acid, tended to decrease. The amounts of several AA‐derived lipids including COX‐catalyzed prostaglandin (PG) D₂ and PGE₂, and LOX‐catalyzed leukotriene (LT) B₄ were increased in clinical mastitic milk. Although subclinical mastitic milk represented similar trend of lipid production to healthy milk, amounts of several lipids such as LTD₄, 14,15‐dihydroxyeicosatrienoic acid, and 14‐epoxyeicosatrienoic acid changed. These findings would be helpful for better understanding of mastitis pathology and give us some insights to develop a new diagnostic and therapeutic strategy.     

Cell proliferation potency is independent of FGF4 signaling in trophoblast stem cells derived from androgenetic embryos

We previously established trophoblast stem cells from mouse androgenetic embryos (AGTS cells). In this study, to further characterize AGTS cells, we compared cell proliferation activity between trophoblast stem (TS) cells and AGTS cells under fibroblast growth factor 4 (FGF4) signaling. TS cells continued to proliferate and maintained mitotic cell division in the presence of FGF4. After FGF4 deprivation, the cell proliferation stopped, the rate of M-phase cells decreased, and trophoblast giant cells formed. In contrast, some of AGTS cells continued to proliferate, and the rate of M-phase cells did not decrease after FGF4 deprivation, although the other cells differentiated into giant cells. RO3306, an ATP competitor that selectively inhibits CDK1, inhibited the cell proliferation of both TS and AGTS cells. Under RO3306 treatment, cell death was induced in AGTS cells but not in TS cells. These results indicate that RO3306 caused TS cells to shift mitotic cell division to endoreduplication but that some of AGTS cells did not shift to endoreduplication and induced cell death. In conclusion, the paternal genome facilitated the proliferation of trophoblast cells without FGF4 signaling.     

Cushing's disease complicated with thrombosis in a dog

Thrombosis is a potential complication of hyperadrenocorticism (HAC) in dogs. An 8-year-old male Beagle diagnosed with pituitary-dependent HAC had complicated with thrombosis in the caudal vena cava and abdominal aorta, which was treated by hypophysectomy and antithrombotic therapy. After hypophysectomy, hypercortisolemia disappeared and the general condition was also significantly improved. Ultrasonography after hypophysectomy revealed that the thrombus remained in the abdominal aorta, but the thrombus in the caudal vena cava had disappeared. However 692 days after the hypophysectomy, the dog had an acute onset of dyspnea and died. Postmortem examination revealed the presence of thrombi in the abdominal aorta and the pulmonary artery. Observations from this case show that HAC dogs must be attention to thrombosis.