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Discovering Genes That Cause Disease
Published in Kenneth L. Brigham, Gene Therapy for Diseases of the Lung, 2020
So are such efforts doomed? In the spirit of recent experience, apparently insurmountable obstacles are still likely to yield to advancing genome technology. For the case of common diseases, the solution will likely be found in one of three approaches: (1) Identification of a prevalent predisposing haplotype (linkage disequilibrium) in a genetically homogeneous population. The recent use of this strategy to clone the gene for diastrophic dysplasia in Finland (21) lends strong support to the concept that such populations allow tracking of a much more refined predisposing region. Counting on such linkage disequilibrium to come to the rescue in a more outbred population may be risky, however. (2) Identification of a syntenic animal model. Animal models of human disease may not necessarily reflect the same predisposing loci, of course; but if genetic linkage analysis indicates that a small syntenic region is contributing relative risk in animals and humans, shifting the analysis to the animal species will be a highly attractive option. The ability to perform selective cross-breeding allows much more precise mapping of a polygene in animal experiments than in humans. (3) If all else fails, the availability of a highly dense transcript map (reducing the hunt for candidate genes to a computer exercise), coupled with powerful methods to search for sequence variation over large numbers of candidate DNA segments (where DNA chip hybridization (22) may greatly speed throughput), may still prevail.
Molecular Genetic Approaches to Obesity
Published in Claude Bouchard, The Genetics of Obesity, 2020
Streamson C. Chua, Rudolph L. Leibel
Molecular genetic linkage maps around two mouse obesity mutations, ob and db, indicate the existence of extensive regions of conserved synteny between the mouse and human genomes in these regions. Around the mouse obese mutation there appears to be a region of at least 20 cM which shows conservation of gene order and distance between proximal mouse chromosome 6 and human chromosome 7q. Two markers, collagen type IV and the skeletal muscle chloride channel (Clc-1), appear to define the extent of the syntenic region. For the mouse diabetes mutation there is a smaller 15-cM region of mouse mid-chromosome 4 with synteny to human chromosome lp. Two other mouse obesity mutations, tub and fat, are located on mouse chromosomes 7 and 8, respectively.10 Since molecular maps around tub and fat are less developed, the exact regions of homology in the human genome are not definitely known. The identification of molecular markers (genes) from a specific human chromosome which flank each of these mouse mutations will pinpoint the region of synteny to the human genome. Molecular maps of such syntenic regions can be used to predict the respective locations of homologous genes between species.22 Such a relationship was exploited recently to demonstrate the likely correspondence of the mouse db to the rat fa mutation.13
Optimizing Reporter Gene Expression for Molecular Magnetic Resonance Imaging
Published in Shoogo Ueno, Bioimaging, 2020
Qin Sun, Frank S. Prato, Donna E. Goldhawk
Magnetosome synthesis is a protein-directed process, beginning with expression of structural genes that encode the required magnetosome components. While the nature of these components is still incompletely understood, progress has been made in many areas. The genomes of numerous MTB have now been sequenced, permitting comparison of conserved gene sequences and synteny.42,43 Despite the breadth of MTB species, there are common genes that specify the main magnetosome structure and approximately two-thirds of these are clustered on a magnetosome genomic island.44 Removal of this cluster of DNA prevents magnetotaxis in the microorganism but is not lethal, demonstrating that magnetosomes likely confer selective advantage(s) rather than compulsory function(s).
The evolution and competitive strategies of Akkermansia muciniphila in gut
Published in Gut Microbes, 2022
Ji-Sun Kim, Se Won Kang, Ju Huck Lee, Seung-Hwan Park, Jung-Sook Lee
Multiple genome alignments were performed to identify the structural differences in the genome. Genome synteny also showed no significant differences between the KGMB strains. However, it was found that there are length variations in the homopolymeric polyguanine (poly G) region in the promoter of fumarate hydratase between type strain KCTC 15667 T and KGMB strains (Figure S1). KGMB strains had a greater number of homopolymeric guanosine repeats, 22–29 mer Gs, compared to the type strain with 18-mer Gs. Fumarate hydratase, also known as fumarase, converts fumaric acid to L-malic acid in the tricarboxylic acid (TCA) cycle, and is a conserved protein in all organisms, from bacteria to humans, with respect to its sequence, structure, and enzymatic activity.37,38 Although the intergenic region (297 bp) of fumarase was identical between the type strain KCTC 15667 T and KGMB strains, differences in the number of poly G repeats in the promoter may cause physiological differences between them.
Population structure of Han population in China revealed by 41 STR loci
Published in Annals of Human Biology, 2020
Weiwei Wu, Deliang Chen, Yanfang Fu, Honglei Hao, Hailun Nan, Dejian Lu
With the increasing number of available forensic markers, it is unavoidable that two or more markers are physically present in the same chromosome (a.k.a. syntenic markers). When using DNA markers that are located on the same chromosome, the forensic community may be concerned about the effect of linkage disequilibrium (LD). In the present study, there are several two to four syntenic STR markers found on 11 different chromosomes (Table S5). The smallest physical distance between the markers is only 3.46 Mb apart (SE33-D6S1043). However, no syntenic STR pairs showed linkage disequilibrium. Therefore, the effect of linkage among the 41 autosomal STR markers can be neglected at the population level. This conclusion agrees with previous reports (Westen et al. 2012; Wu et al. 2014; Liu et al. 2016). Notably, genetic linkage is likely to have an impact on profile probability calculations for most related individuals even though linkage equilibrium was assumed (Gill et al. 2012).
Evolutionary Underpinnings of Innate-Like T Cell Interactions with Cancer
Published in Immunological Investigations, 2019
Maureen Banach, Jacques Robert
Although CD1d predominantly performs immune functions via stimulation of iTCR, other MHC class I molecules can ligate with both TCR and non-TCR receptors. For example, human HLA-E and its murine homolog Qa-1b interact with M. tuberculosis-associated TCR and with the members of NKG2-CD94 NK receptors. Importantly, the ligation of HLA-E/Qa-1b to NKG2A-CD94 or NKG2C-CD94 confers disparate immune responses: inhibitory and activating signals, respectively (Braud et al., 1998; Vance et al., 1998). Analogously, XNC10 interactions may operate beyond TCR ligation. The identification of non-TCRs in Xenopus is limited by high evolutionary plasticity and minimal sequence similarities (Ohta and Flajnik, 2015). Still, several putative activating and inhibitory NK-like receptors in Xenopus have been identified (Guselnikov et al., 2010; Ohta et al., 2006; Yoder and Litman, 2011). In addition, X. tropicalis and X. laevis genome harbor 75 members of activating and inhibitory Fc-like receptors (Guselnikov et al., 2008). The genome synteny studies based on the newly released assembly will facilitate the discovery of additional non-TCR receptors.