Mammalian genome : official journal of the International Mammalian Genome Society最新文献

{"title":"Methods for vascularization and perfusion of tissue organoids.","authors":"Hannah A Strobel,&nbsp;Sarah M Moss,&nbsp;James B Hoying","doi":"10.1007/s00335-022-09951-2","DOIUrl":"https://doi.org/10.1007/s00335-022-09951-2","url":null,"abstract":"<p><p>Tissue organoids or \"mini organs\" can be invaluable tools for understanding health and disease biology, modeling tissue dynamics, or screening potential drug candidates. Effective vascularization of these models is critical for truly representing the in vivo tissue environment. Not only is the formation of a vascular network, and ultimately a microcirculation, essential for proper distribution and exchange of oxygen and nutrients throughout larger organoids, but vascular cells dynamically communicate with other cells to modulate overall tissue behavior. Additionally, interstitial fluid flow, mediated by a perfused microvasculature, can have profound influences on tissue biology. Thus, a truly functionally and biologically relevant organoid requires a vasculature. Here, we review existing strategies for fabricating and incorporating vascular elements and perfusion within tissue organoids.</p>","PeriodicalId":412165,"journal":{"name":"Mammalian genome : official journal of the International Mammalian Genome Society","volume":" ","pages":"437-450"},"PeriodicalIF":2.5,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40328196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A deletion containing a CTCF-element in intron 8 of the Bbs7 gene is partially responsible for juvenile obesity in the Berlin Fat Mouse.","authors":"Florian Krause,&nbsp;Kourosh Mohebian,&nbsp;Manuel Delpero,&nbsp;Deike Hesse,&nbsp;Ralf Kühn,&nbsp;Danny Arends,&nbsp;Gudrun A Brockmann","doi":"10.1007/s00335-021-09938-5","DOIUrl":"https://doi.org/10.1007/s00335-021-09938-5","url":null,"abstract":"<p><p>The Berlin Fat Mouse Inbred (BFMI) line is a model for juvenile obesity. Previous studies on crosses between BFMI and C57Bl/6N (B6N) have identified a recessive defect causing juvenile obesity on chromosome 3 (jObes1). Bbs7 was identified as the most likely candidate gene for the observed effect. Comparative sequence analysis showed a 1578 bp deletion in intron 8 of Bbs7 in BFMI mice. A CTCF-element is located inside this deletion. To investigate the functional effect of this deletion, it was introduced into B6N mice using CRISPR/Cas9. Two mice containing the target deletion were obtained (B6N Bbs7^emI8∆1 and Bbs7^emI8∆2) and were subsequently mated to BFMI and B6N to generate two families suitable for complementation. Inherited alleles were determined and body composition was measured by quantitative magnetic resonance. Evidence for a partial complementation (13.1-15.1%) of the jObes1 allele by the CRISPR/Cas9 modified B6N Bbs7^emI8∆1 and Bbs7^emI8∆2 alleles was found. Mice carrying the complementation alleles had a 23-27% higher fat-to-lean ratio compared to animals which have a B6N allele (P_{(Bbs7emI8∆1)} = 4.25 × 10^-7; P_{(Bbs7emI8∆2)} = 3.17 × 10^-5). Consistent with previous findings, the recessive effect of the BFMI allele was also seen for the B6N Bbs7^emI8∆1 and Bbs7^emI8∆2 alleles. However, the effect size of the B6N Bbs7^emI8∆1 and Bbs7^emI8∆2 alleles was smaller than the BFMI allele, and thus showed only a partial complementation. Findings suggest additional variants near Bbs7 in addition to or interacting with the deletion in intron 8.</p>","PeriodicalId":412165,"journal":{"name":"Mammalian genome : official journal of the International Mammalian Genome Society","volume":" ","pages":"465-470"},"PeriodicalIF":2.5,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9360062/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39604454","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polygenic control of the wavy coat of the NCT mouse: involvement of an intracisternal A particle insertional mutation of the protease, serine 53 (Prss53) gene, and a modifier gene.","authors":"Masayuki Mori,&nbsp;Chang Liu,&nbsp;Takahiro Yoshizawa,&nbsp;Hiroki Miyahara,&nbsp;Jian Dai,&nbsp;Yuichi Igarashi,&nbsp;Xiaoran Cui,&nbsp;Ying Li,&nbsp;Xiaojing Kang,&nbsp;Keiichi Higuchi","doi":"10.1007/s00335-021-09926-9","DOIUrl":"https://doi.org/10.1007/s00335-021-09926-9","url":null,"abstract":"<p><p>The Nakano cataract mouse (NCT) manifests a wavy coat for their first hair as a genetic trait. In this study, we explored the molecular genetic basis of the wavy coat. We revealed by crossing experiments that the wavy coat is controlled by a major gene on chromosome 7 of NCT, homozygosity of which is a prerequisite for developing the wavy coat, and by a gene on chromosome 9 with a minor effect to reinforce the manifestation of the trait. In humans, a polymorphism of the protease, serine 53 (PRSS53) gene on the homologous chromosome is known to be associated with curly scalp hair. We then investigated the Prss53 gene and discovered that NCT has an insertion of an intracisternal A particle element in the first intron of the gene. Nevertheless, the expression of the Prss53 is not altered in the NCT skin both in transcript and protein levels. Subsequently, we created C57BL/6J-Prss53^em1 knockout mice and found that these mice manifest vague wavy coats. A portion of backcross and intercross mice between the C57BL/6J-Prss53^em1 and NCT manifested intense or vague wavy coats. These findings demonstrate the polygenic nature of the wavy coat of NCT and Prss53 knockout mice and highlight the similarity of the trait to the curly hair of humans associated with the PRSS53 alteration.</p>","PeriodicalId":412165,"journal":{"name":"Mammalian genome : official journal of the International Mammalian Genome Society","volume":" ","pages":"451-464"},"PeriodicalIF":2.5,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39852151","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular determination of progesterone receptor's PROGINS allele (Alu insertion) and its association with the predisposition and susceptibility to polycystic ovary syndrome (PCOS).","authors":"Rashid Mir,&nbsp;Malik A Altayar,&nbsp;Abdullah Hamadi,&nbsp;Faris J Tayeb,&nbsp;Nizar H Saeedi,&nbsp;Mohammed M Jalal,&nbsp;Jameel Barnawi,&nbsp;Sanad E Alshammari,&nbsp;Nabil Mtiraoui,&nbsp;Mohammed Eltigani M Ali,&nbsp;Faisel M Abuduhier,&nbsp;Mohammad Fahad Ullah","doi":"10.1007/s00335-021-09941-w","DOIUrl":"https://doi.org/10.1007/s00335-021-09941-w","url":null,"abstract":"<p><p>Polycystic ovary syndrome, previously known as Stein-Leventhal syndrome, is associated with altered reproductive endocrinology, predisposing a young woman towards the risk of PCOS. It has a prevalence of 6-20% among the reproductive-age women. Progesterone is a key hormone in the pathophysiology of PCOS and patients show diminished response (progesterone resistance), implicating the role of progesterone receptor (PR) as a factor in the disease etiology and prognosis. In this case-control study, we have used mutation-specific PCR (confirmed by Sanger sequencing) to detect the presence of a pathologically significant PR polymorphic variant called as PROGINS. The variant has an Alu insertion in intron G and has two SNPs in exon 4 and exon 5, with all the three aberrations in complete disequilibrium. Our results demonstrated a statistically significant difference in the frequencies of PROGINS between the PCOS patients and healthy controls (p = 0.047). The frequencies of the genotypes CC (A1/A1), CT (A1/A2), and TT (A2/A2) in patients were 74.50%, 20.58%, and 4.90%, and in healthy controls they were 87.28%, 11%, and 1.69%, respectively. Our results put forward two determining factors with regard to PCOS: (i) the frequency of PROGINS allele was significantly higher among PCOS patients compared to the healthy matched controls (0.15 vs 0.07) in the studied population, (ii) the PROGIN allele was significantly associated with the lower levels of serum progesterone in PCOS patients (p < 0.003). The findings are conspicuous as these relate the PROGINS variant to the increased susceptibility of PCOS and might explain the progesterone resistance in patients.</p>","PeriodicalId":412165,"journal":{"name":"Mammalian genome : official journal of the International Mammalian Genome Society","volume":" ","pages":"508-516"},"PeriodicalIF":2.5,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39797704","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNAs PSMG3-AS1 and MEG3 negatively regulate each other to participate in endometrial carcinoma cell proliferation.","authors":"Shuai Huang,&nbsp;Jiankun Chen,&nbsp;Xuexiao Gao,&nbsp;Zhiyuan Shang,&nbsp;Xiao Ma,&nbsp;Xia Zhang,&nbsp;Jiayang Li,&nbsp;Ruoyun Yin,&nbsp;Xiaojing Meng","doi":"10.1007/s00335-021-09931-y","DOIUrl":"https://doi.org/10.1007/s00335-021-09931-y","url":null,"abstract":"<p><p>Endometrial carcinoma (EC), also known as corpus cancer or corpus uterine cancer, is the most frequently diagnosed genital cancer among women in developed countries. Our preliminary RNA-seq analysis revealed the inverse correlation between the expression of PSMG3-AS1 and MEG3 across EC tissues, indicating the possible interaction between them. This study aimed to explore the interaction between two long non-coding RNAs (lncRNAs) PSMG3-AS1 and MEG3 in EC. Investigation of the interaction between two lncRNAs in cancer biology is a novel topic. The expression of PSMG3-AS1 and MEG3 in EC and paired non-tumor tissues from 60 EC patients were determined by RT-qPCR. Correlations between them were analyzed by Pearson's correlation coefficient. PSMG3-AS1 and MEG3 were overexpressed in EC cells to study the relationship between them. The roles of PSMG3-AS1 and MEG3 in regulating the proliferation of EC cells were assessed by CCK-8 assay. PSMG3-AS1 was upregulated, while MEG3 was downregulated in EC. Across EC tissues, the expression of PSMG3-AS1 and MEG3 were inversely correlated. In EC cells, overexpression of PSMG3-AS1 and MEG3 resulted in the downregulation of each other. In cell proliferation assay, PSMG3-AS1 promoted cell proliferation, and MEG3 inhibited cell proliferation. Moreover, the proliferation rate of cells co-transfected with PSMG3-AS1 and MEG3 expression vectors was not different from that in cells without transfections. In conclusion, PSMG3-AS1 and MEG3 may negatively regulate each other to regulate EC cell proliferation.</p>","PeriodicalId":412165,"journal":{"name":"Mammalian genome : official journal of the International Mammalian Genome Society","volume":" ","pages":"502-507"},"PeriodicalIF":2.5,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39869719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Best practices for analyzing imputed genotypes from low-pass sequencing in dogs.","authors":"Reuben M Buckley,&nbsp;Alex C Harris,&nbsp;Guo-Dong Wang,&nbsp;D Thad Whitaker,&nbsp;Ya-Ping Zhang,&nbsp;Elaine A Ostrander","doi":"10.1007/s00335-021-09914-z","DOIUrl":"https://doi.org/10.1007/s00335-021-09914-z","url":null,"abstract":"<p><p>Although DNA array-based approaches for genome-wide association studies (GWAS) permit the collection of thousands of low-cost genotypes, it is often at the expense of resolution and completeness, as SNP chip technologies are ultimately limited by SNPs chosen during array development. An alternative low-cost approach is low-pass whole genome sequencing (WGS) followed by imputation. Rather than relying on high levels of genotype confidence at a set of select loci, low-pass WGS and imputation rely on the combined information from millions of randomly sampled low-confidence genotypes. To investigate low-pass WGS and imputation in the dog, we assessed accuracy and performance by downsampling 97 high-coverage (> 15×) WGS datasets from 51 different breeds to approximately 1× coverage, simulating low-pass WGS. Using a reference panel of 676 dogs from 91 breeds, genotypes were imputed from the downsampled data and compared to a truth set of genotypes generated from high-coverage WGS. Using our truth set, we optimized a variant quality filtering strategy that retained approximately 80% of 14 M imputed sites and lowered the imputation error rate from 3.0% to 1.5%. Seven million sites remained with a MAF > 5% and an average imputation quality score of 0.95. Finally, we simulated the impact of imputation errors on outcomes for case-control GWAS, where small effect sizes were most impacted and medium-to-large effect sizes were minorly impacted. These analyses provide best practice guidelines for study design and data post-processing of low-pass WGS-imputed genotypes in dogs.</p>","PeriodicalId":412165,"journal":{"name":"Mammalian genome : official journal of the International Mammalian Genome Society","volume":" ","pages":"213-229"},"PeriodicalIF":2.5,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8913487/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39399139","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mouse resources at the RIKEN BioResource Research Center and the National BioResource Project core facility in Japan.","authors":"Saori Mizuno-Iijima,&nbsp;Toshiaki Nakashiba,&nbsp;Shinya Ayabe,&nbsp;Hatsumi Nakata,&nbsp;Fumio Ike,&nbsp;Noriko Hiraiwa,&nbsp;Keiji Mochida,&nbsp;Atsuo Ogura,&nbsp;Hiroshi Masuya,&nbsp;Shoko Kawamoto,&nbsp;Masaru Tamura,&nbsp;Yuichi Obata,&nbsp;Toshihiko Shiroishi,&nbsp;Atsushi Yoshiki","doi":"10.1007/s00335-021-09916-x","DOIUrl":"https://doi.org/10.1007/s00335-021-09916-x","url":null,"abstract":"<p><p>The RIKEN BioResource Research Center (BRC) was established in 2001 as a comprehensive biological resource center in Japan. The Experimental Animal Division, one of the BRC infrastructure divisions, has been designated as the core facility for mouse resources within the National BioResource Project (NBRP) by the Japanese government since FY2002. Our activities regarding the collection, preservation, quality control, and distribution of mouse resources have been supported by the research community, including evaluations and guidance on advancing social and research needs, as well as the operations and future direction of the BRC. Expenditure for collection, preservation, and quality-control operations of the BRC, as a national core facility, has been funded by the government, while distribution has been separately funded by users' reimbursement fees. We have collected over 9000 strains created mainly by Japanese scientists including Nobel laureates and researchers in cutting-edge fields and distributed mice to 7000 scientists with 1500 organizations in Japan and globally. Our users have published 1000 outstanding papers and a few dozen patents. The collected mouse resources are accessible via the RIKEN BRC website, with a revised version of the searchable online catalog. In addition, to enhance the visibility of useful strains, we have launched web corners designated as the \"Mouse of the Month\" and \"Today's Tool and Model.\" Only high-demand strains are maintained in live colonies, while other strains are cryopreserved as embryos or sperm to achieve cost-effective management. Since 2007, the RIKEN BRC has built up a back-up facility in the RIKEN Harima branch to protect the deposited strains from disasters. Our mice have been distributed with high quality through the application of strict microbial and genetic quality control programs that cover a globally accepted pathogens list and mutated alleles generated by various methods. Added value features, such as information about users' publications, standardized phenotyping data, and genome sequences of the collected strains, are important to facilitate the use of our resources. We have added and disseminated such information in collaboration with the NBRP Information Center and the NBRP Genome Information Upgrading Program. The RIKEN BRC has participated in international mouse resource networks such as the International Mouse Strain Resource, International Mouse Phenotyping Consortium, and Asian Mouse Mutagenesis and Resource Association to facilitate the worldwide use of high-quality mouse resources, and as a consequence it contributes to reproducible life science studies and innovation around the globe.</p>","PeriodicalId":412165,"journal":{"name":"Mammalian genome : official journal of the International Mammalian Genome Society","volume":" ","pages":"181-191"},"PeriodicalIF":2.5,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8445257/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39445011","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rat Models of Human Diseases and Related Phenotypes: A Novel Inventory of Causative Genes.","authors":"Claude Szpirer","doi":"10.1007/s00335-021-09876-2","DOIUrl":"https://doi.org/10.1007/s00335-021-09876-2","url":null,"abstract":"<p><p>The laboratory rat (Rattus norvegicus) has been used for a long time as the model of choice in several biomedical disciplines. In 2020, I made an inventory of rat genes that had been identified as underlying diseases or playing a key role in critical biological processes that are altered in diseases. Over 350 genes could be found, a significant number of which have similar effects in rat and humans (Szpirer in J Biomed Sci 27:84-155, 2020). However, a few rat disease genes were unintentionally overlooked; in addition, since this review was published, numerous rat genes were inactivated by targeted mutations, revealing their potential role in diseases. It thus seems appropriate to update these data, which is the aim of this paper.</p>","PeriodicalId":412165,"journal":{"name":"Mammalian genome : official journal of the International Mammalian Genome Society","volume":" ","pages":"88-90"},"PeriodicalIF":2.5,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s00335-021-09876-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39117611","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mouse models of aneuploidy to understand chromosome disorders.","authors":"Justin Tosh, Victor Tybulewicz, Elizabeth M C Fisher","doi":"10.1007/s00335-021-09930-z","DOIUrl":"10.1007/s00335-021-09930-z","url":null,"abstract":"<p><p>An organism or cell carrying a number of chromosomes that is not a multiple of the haploid count is in a state of aneuploidy. This condition results in significant changes in the level of expression of genes that are gained or lost from the aneuploid chromosome(s) and most cases in humans are not compatible with life. However, a few aneuploidies can lead to live births, typically associated with deleterious phenotypes. We do not understand why phenotypes arise from aneuploid syndromes in humans. Animal models have the potential to provide great insight, but less than a handful of mouse models of aneuploidy have been made, and no ideal system exists in which to study the effects of aneuploidy per se versus those of raised gene dosage. Here, we give an overview of human aneuploid syndromes, the effects on physiology of having an altered number of chromosomes and we present the currently available mouse models of aneuploidy, focusing on models of trisomy 21 (which causes Down syndrome) because this is the most common, and therefore, the most studied autosomal aneuploidy. Finally, we discuss the potential role of carrying an extra chromosome on aneuploid phenotypes, independent of changes in gene dosage, and methods by which this could be investigated further.</p>","PeriodicalId":412165,"journal":{"name":"Mammalian genome : official journal of the International Mammalian Genome Society","volume":" ","pages":"157-168"},"PeriodicalIF":0.0,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8913467/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39577920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Asian Mouse Mutagenesis Resource Association (AMMRA): mouse genetics and laboratory animal resources in the Asia Pacific.","authors":"Hsian-Jean Chin,&nbsp;Michael S Dobbie,&nbsp;Xiang Gao,&nbsp;James E Hennessy,&nbsp;Ki-Hoan Nam,&nbsp;Je Kyung Seong,&nbsp;Toshihiko Shiroishi,&nbsp;Toru Takeo,&nbsp;Atsushi Yoshiki,&nbsp;Jing Zao,&nbsp;Chi-Kuang Leo Wang","doi":"10.1007/s00335-021-09912-1","DOIUrl":"https://doi.org/10.1007/s00335-021-09912-1","url":null,"abstract":"<p><p>The Asian Mouse Mutagenesis Resource Association (AMMRA) is a non-profit organization consisting of major resource and research institutions with rodent expertise from within the Asia Pacific region. For more than a decade, aiming to support biomedical research and stimulate international collaboration, AMMRA has always been a friendly and passionate ally of Asian and Australian member institutions devoted to sharing knowledge, exchanging resources, and promoting biomedical research. AMMRA is also missioned to global connection by working closely with the consortiums such as the International Mouse Phenotyping Consortium and the International Mouse Strain Resource. This review discusses the emergence of AMMRA and outlines its many roles and responsibilities in promoting, assisting, enriching research, and ultimately enhancing global life science research quality.</p>","PeriodicalId":412165,"journal":{"name":"Mammalian genome : official journal of the International Mammalian Genome Society","volume":" ","pages":"192-202"},"PeriodicalIF":2.5,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8418786/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39384195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}