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Metagonimus
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Jong-Yil Chai, Bong-Kwang Jung
M. miyatai is morphologically unique in having two markedly separated testes from each other, with the posterior one located very close to the posterior body wall of the worm, vitelline follicles never distributing beyond the posterior testis, and the egg size, which is intermediate between those of M. yokogawai and M. takahashii.9,20,29,36M. miyatai is also genetically distinct from M. yokogawai and M. takahashii as shown by distinct polymerase chain reaction–restriction fragment length polymorphism (PCR-RFLP),59 random amplified polymorphic DNA (RAPD),60 chromosome,61 and simple sequence repeat anchored-PCR (SSR-PCR) patterns.27
Genetic Resources of Syzygium cumini in India
Published in K. N. Nair, The Genus Syzygium, 2017
S. K. Malik, Rekha Chaudhury, Vartika Srivastava, Sanjay Singh
Preliminary studies on molecular characterization of jamun have also been attempted at ICAR-CISH, and eight accessions were analyzed using random amplification of polymorphic DNA (RAPD) techniques where 14 primers were used, revealing the distinctness of J-36 and J-22 from other accessions (Anonymous 2010). Shakya et al. (2010) analyzed eight jamun accessions being maintained at ICAR-CISH for genetic diversity using RAPD and simple sequence repeat (SSR) markers. The accessions belonging to different geographical regions were grouped in separate clusters indicating interpopulation differences. They reported that OPZ9 and OPA12 primers can detect very small differences between these selections. Khan et al. (2011) analyzed 16 genotypes of jamun collected from three agroecological regions using RAPD markers. The study revealed a high level of polymorphism (47.69%–74.87%) in the sample populations that was correlated with the population size.
Hypertension genetics: candidate genetic loci, 'intermediate' phenotypes, and genome-wide searches for susceptibility loci
Published in H. Gavras, The Year in Hypertension 2004, 2004
CLAYTON SMILEY, SHAGUN CHOPRA, DANIEL T O'CONNOR
search for trait susceptibility loci throughout the genome. Such searches are possible in relative pairs, typically as found in sibships or nuclear families. Because siblings share large regions of the genome undisrupted by meioses (indeed, in genetic terms siblings are separated by only a single meiosis), a relatively small number of genetic markers (typically -300-400 highly heterozygous microsatellite [simple sequence repeat] polymorphisms) can serve to mark loci in chromosomal locations across the genome (22 autosomes and X chromosome). Such studies evaluate 'linkage' (co- segregation) of marker locus with a trait, and typically report evidence of linkage in a LOD score. Because the sib-pair linkage method may be less statistically powerful than allelic association studies at a candidate locus, especially if there is locus heterogeneity in trait determination, large numbers of sib pairs are typically required for adequate power in such linkage studies.
Development and characterization of gamma ray and EMS induced mutants for powdery mildew resistance in blackgram
Published in International Journal of Radiation Biology, 2023
Murugesan Tamilzharasi, Dharmalingam Kumaresan, Venkatesan Thiruvengadam, Jegadeesan Souframanien, T. K. S. Latha, N. Manikanda Boopathi, Palaniappan Jayamani
In an earlier study, random amplified polymorphic DNA (RAPD) and inter simple sequence repeat (ISSR) markers were used to study the DNA polymorphism and diversity among gamma ray induced mutants of blackgram (Arulbalachandran et al. 2010). In the present study, SSR markers were used to study genetic diversity among the mutants and the susceptible parent CO 6 which were grouped into different clusters. The akin findings were reported by Ramchander et al (2022) in rice. The mutants PM 21 with PM 54 (31.62) and PM 56 (34.64) had low dissimilarity. The same trend was applied for PM 20 with PM 42 (38.72) and PM 53 (41.23). A higher proportion of variability was noticed in-between CO 6 and PM 21 which had a maximum dissimilarity value of 81.24 (Supplementary File 4). This is in line with the previous report on DNA polymorphism and clustering of gamma ray induced mutants (Ramchander et al. 2022).
Combining inhibition of immune checkpoints and PARP: rationale and perspectives in cancer treatment
Published in Expert Opinion on Therapeutic Targets, 2022
Martina Catalano, Luigi Francesco Iannone, Federica Cosso, Daniele Generali, Enrico Mini, Giandomenico Roviello
Mismatch repair consists of DNA mismatch repair (MMR) systems that involve proteins that recognize and repair erroneous insertion, deletion, and mis-incorporation of bases caused by DNA polymerase during the DNA replication [10]. In non-tumoral cells, the repair system is formed by four main proteins: MutL Homolog 1 (MLH1), MutS Homolog 2 (MSH2), MutS Homolog 6 (MSH6), and Post Meiotic Segregation increased 2 (PMS2) [10]. Germinal and/or somatic deleterious variants of these proteins lead to the failure and inactivation of the MMR system with a consequent accumulation of high rate of mutations, mainly in microsatellites, detectable as microsatellite instability (MSI) [11]. Therefore, the instability of microsatellites represents the molecular phenotype of the DNA repair system deficit. Microsatellites also defined as short tandem repeats (STR) or Simple Sequence Repeat (SSRs), are short repeating sequences of 1–6 nucleotides [11].
The role of neuraminidase 1 (NEU1) in cytokine release by primary mouse mesangial cells and disease outcomes in murine lupus nephritis
Published in Autoimmunity, 2021
Jessalyn Rodgers, Kamala Sundararaj, Evelyn Bruner, Bethany Wolf, Tamara K. Nowling
B6 Neu1+/- and B6.SLE1/2/3 mice were bred to generate B6.SLE1/2/3 Neu1+/- mice and backcrossed for five generations before being used in the study. Tail DNA was extracted at weaning and used to genotype the mice for Neu1 and the three NZM2410 lupus susceptibility loci Sle1, Sle2 and Sle3. PCR for Neu1 was performed following a protocol supplied by the lab of Dr. Alessandra d’Azzo using multiplex primers MNTG-1, MNTG-2 and LacZ to detect the wild-type allele (MNTG-1 and MNTG-2), and knockout allele (MNTG-1 and LacZ). PCR for the three congenic SLE (Sle1, Sle2, and Sle3) intervals was performed using primers for simple-sequence repeat markers essentially as reported previously [18–21]. Primer sequences and expected PCR amplicon sizes for each genotype are provided in Table 1. Prior to being used in the genetic study, mice were confirmed to have NZM2410-derived genotype for the three SLE loci at nine out of the eleven SLE susceptibility alleles and C57BL/6J at D7MIT40 as expected. D7MIT30 and D7MIT31 at the proximal end of chromosome 7 were reported to be NZM2410-derived [19,20]. However, our genotyping results indicated that all B6.SLE1/2/3 mice, including the breeding pairs purchased from Jackson Laboratories were homozygous for the C57BL/6J strain. DNA from NZM2410 mice and C57BL/6J DNA were used as controls. Tan coat colour and pink eye colour were also used as phenotypic indicators of homozygous NZM2410 genotype at Chromosome 4b loci and Chromosome 7 p loci, respectively, in the B6.SLE1/2/3 mice.