The Effects of Visual Object Size in The Depth Perception in KM Mouse

Whether mice perceive the depth of space dependent on the visual size of object targets was explored when visual cues such as perspective and partial occlusion in space were excluded. A mouse was placed on a platform the height of which is adjustable. The platform located inside a box in which all other walls were dark exception its bottom through that light was projected as a sole visual cue. The visual object cue was composed of 4x4 grids to allow a mouse estimating the distance of the platform relative to the grids. Three sizes of grids reduced in a proportion of 2/3 and seven distances with an equal interval between the platform and the grids at the bottom were applied in the experiments. The duration of a mouse staying on the platform at each height was recorded when the different sizes of the grids were presented randomly to test whether the Judgment of the mouse for the depth of the platform from the bottom was affected by the size information of the visual target. The results from all conditions of three object sizes show that time of mice staying on the platform became longer with the increase in height. In distance of 20 similar to 30 cm, the mice did not use the size information of a target to judge the depth, while mainly used the information of binocular disparity. In distance less than 20 cm or more than 30 cm, however, especially in much higher distance 50 cm, 60 cm and 70 cm, the mice were able to use the size information to do so in order to compensate the lack of binocular disparity information from both eyes. Because the mice have only 1/3 of the visual field that is binocular. This behavioral paradigm established in the current study is a useful model and can be applied to the experiments using transgenic mouse as an animal model to investigate the relationships between behaviors and gene functions.

Detection of hepatitis B virus markers using a biosensor based on imaging ellipsometry

A biosensor based on imaging ellipsometry (BIE) has been developed and validated in 169 patients for detecting five markers of hepatitis B virus (HBV) infection. The methodology has been established to pave the way for clinical diagnosis, including ligand screening, determination of the sensitivity, set-up of cut-off values (CoVs) and comparison with other clinical methods. A matrix assay method was established for ligand screening. The CoVs of HBV markers were derived with the help of receiver operating characteristic curves. Enzyme-linked immunosorbent assay (ELISA) was the reference method. Ligands with high bioactivity were selected and sensitivities of 1 ng/mL and 1 IU/mL for hepatitis B surface antigen (HBsAg) and surface antibody (anti-HBs) were obtained respectively. The CoVs of HBsAg, anti-HBs, hepatitis B e antigen, hepatitis B e antibody and core antibody were as follows: 15%, 18%, 15%, 20% and 15%, respectively, which were the percentages over the values of corresponding ligand controls. BIE can simultaneously detect up to five markers within 1 h with results in acceptable agreement with ELISA, and thus shows a potential for diagnosing hepatitis B with high throughput.

Chromosome painting in the long-tailed field mouse provides insights into the ancestral murid karyotype

We report on the hybridization of mouse chromosomal paints to Apodemus sylvaticus, the long-tailed field mouse. The mouse paints detected 38 conserved segments in the Apodemus karyotype. Together with the species reported here there are now six species of rodents mapped with Mus musculus painting probes. A parsimony analysis indicated that the syntenies of nine M. musculus chromosomes were most likely already formed in the muroid ancestor: 3, 4, 7, 9, 14, 18, 19, X and Y. The widespread occurrence of syntenic segment associations of mouse chromosomes 1/17, 2/13, 7/19, 10/17, 11/16, 12/17 and 13/15 suggests that these associations were ancestral syntenies for muroid rodents. The muroid ancestral karyotype probably had a diploid number of about 2n = 54. It would be desirable to have a richer phylogenetic array of species before any final conclusions are drawn about the Muridae ancestral karyotype. The ancestral karyotype presented here should be considered as a working hypothesis. Copyright (C) 2004 S. Karger AG, Basel.

Features and trend of loss of promoter-associated CpG islands in the human and mouse genomes

CpG islands (CGIs) are often considered as gene markers, but the number of CGIs varies among mammalian genomes that have similar numbers of genes. In this study, we investigated the distribution of CGIs in the promoter regions of 3,197 human-mouse ortholo

Characterization and Comparison of the Tissue-Related Modules in Human and Mouse

Background: Due to the advances of high throughput technology and data-collection approaches, we are now in an unprecedented position to understand the evolution of organisms. Great efforts have characterized many individual genes responsible for the interspecies divergence, yet little is known about the genome-wide divergence at a higher level. Modules, serving as the building blocks and operational units of biological systems, provide more information than individual genes. Hence, the comparative analysis between species at the module level would shed more light on the mechanisms underlying the evolution of organisms than the traditional comparative genomics approaches. Results: We systematically identified the tissue-related modules using the iterative signature algorithm (ISA), and we detected 52 and 65 modules in the human and mouse genomes, respectively. The gene expression patterns indicate that all of these predicted modules have a high possibility of serving as real biological modules. In addition, we defined a novel quantity, "total constraint intensity,'' a proxy of multiple constraints (of co-regulated genes and tissues where the co-regulation occurs) on the evolution of genes in module context. We demonstrate that the evolutionary rate of a gene is negatively correlated with its total constraint intensity. Furthermore, there are modules coding the same essential biological processes, while their gene contents have diverged extensively between human and mouse. Conclusions: Our results suggest that unlike the composition of module, which exhibits a great difference between human and mouse, the functional organization of the corresponding modules may evolve in a more conservative manner. Most importantly, our findings imply that similar biological processes can be carried out by different sets of genes from human and mouse, therefore, the functional data of individual genes from mouse may not apply to human in certain occasions.

Proteomic Analysis of Proteins Involved in Spermiogenesis in Mouse

Spermiogenesis is a unique process in mammals during which haploid round spermatids mature into spermatozoa in the testis. Its successful completion is necessary for fertilization and its malfunction is an important cause of male infertility. Here, we report the high-confidence identification of 2116 proteins in mouse haploid germ cells undergoing spermiogenesis: 299 of these were testis-specific and 155 were novel. Analysis of these proteins showed many proteins possibly functioning in unique processes of spermiogenesis. Of the 84 proteins annotated to be involved in vesicle-related events, VAMP4 was shown to be important for acrosome biogenesis by in vivo knockdown experiments. Knockdown of VAMP4 caused defects of acrosomal vesicle fusion and significantly increased head abnormalities in spermatids from testis and sperm from the cauda epididymis. Analysis of chromosomal distribution of the haploid genes showed underrepresentation on the X chromosome and overrepresentation on chromosome 11, which were due to meiotic sex chromosome inactivation and expansion of testis-expressed gene families, respectively. Comparison with transcriptional data showed translational regulation during spermiogenesis. This characterization of proteins involved in spermiogenesis provides an inventory of proteins useful for understanding the mechanisms of male infertility and may provide candidates for drug targets for male contraception and male infertility.

Genomic organization and sequence analysis of the vomeronasal receptor V2R genes in mouse genome

Two multigene superfamilies, named V1R and V2R, encoding seven-transmembrane-domain G-protein coupled receptors (GPCRs) have been identified as pheromone receptors in mammals. Three V2R gene families have been described in mouse and rat. Here we screened

Molecular genetic basis for the rhino mouse from Chinese KM subcolony

Both the rhino mouse and hairless mouse resulted from hairless gene mutation, but they show different phenotypes of skin physiology. The rhino mouse has more similar histological characters to human papular alopecia. Therefore rhino mouse is a good experimental animal model for human papular alopecia. This study reports a hairless mouse named rhino KIZ, arose from KM colony in Kunming Institue of Zoology, by systematic studies on morphology, skin histopathology, gene sequence, pedigree and protein domain analysis. The results demonstrate that a C-to-T transition in exon 11 of hr gene (The mutant gene has been applied for a Chinese patent (patent No. 03135280)) results in the rhino KIZ. The rhino KIZ with clear genetic mechanism will be a useful animal model.

HSPC117 deficiency in cloned embryos causes placental abnormality and fetal death

Somatic cell nuclear transfer (SCNT) has been successfully used in many species to produce live cloned offspring, albeit with low efficiency. The low frequency of successful development has usually been ascribed to incomplete or inappropriate reprogramming of the transferred nuclear genome. Elucidating the genetic differences between normal fertilized and cloned embryos is key to understand the low efficiency of SCNT. Here, we show that expression of HSPC117, which encodes a hypothetical protein of unknown function, was absent or very low in cloned mouse blastocysts. To investigate the role of HSPC117 in embryo development, we knocked-down this gene in normal fertilized embryos using RNA interference. We assessed the post-implantation survival of HSPC117 knock-down embryos at 3 stages: E9 (prior to placenta formation); E12 (after the placenta was fully functional) and E19 (post-natal). Our results show that, although siRNA-treated in vivo fertilized/produced (IVP) embryos could develop to the blastocyst stage and implanted without any difference from control embryos, the knock-down embryos showed substantial fetal death, accompanied by placental blood clotting, at E12. Furthermore, comparison of HSPC117 expression in placentas of nuclear transfer (NT), intracytoplasmic sperm injection (ICSI) and IVP embryos confirmed that HSPC117 deficiency correlates well with failures in embryo development: all NT embryos with a fetus, as well as IVP and ICSI embryos, had normal placental HSPC117 expression while those NT embryos showing reduced or no expression of HSPC117 failed to form a fetus. In conclusion, we show that HSPC117 is an important gene for post-implantation development of embryos, and that HSPC117 deficiency leads to fetal abnormalities after implantation, especially following placental formation. We suggest that defects in HSPC117 expression may be an important contributing factor to loss of cloned NT embryos in vivo. (C) 2010 Elsevier Inc. All rights reserved.