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Order Reovirales
Published in Paul Pumpens, Peter Pushko, Philippe Le Mercier, Virus-Like Particles, 2022
Paul Pumpens, Peter Pushko, Philippe Le Mercier
Then, a series of four potent insertion vectors was constructed on the basis of the VP3 gene (Tanaka et al. 1995) in accordance with the deletion mapping data (Le Blois et al. 1991). The insertion of 12 N-terminal aa residues of the phage T7 capsid protein into the internal VP3 regions or the addition of 13 aa of the binding domain of the protein to cellular receptors from bovine leukemia virus (BLV) glycoprotein gp51, which corresponded to aa 155–167 of the BLV gp51, to the C-terminus of VP3 did not prevent the formation of the BTV CLPs, if the VP7 was provided (Tanaka et al. 1995).
Translation
Published in Paul Pumpens, Single-Stranded RNA Phages, 2020
Berkhout and van Duin (1985) approved directly the molecular mechanism of the polarity phenomenon. They performed the deletion mapping on the cloned MS2 cDNA and showed that the ribosomal binding site of the replicase gene was masked really by a long-distance base pairing to an internal coat gene. The removal of the internal coat gene region led to uncoupled replicase synthesis. Therefore, the gene engineering approach confirmed structurally the original polarity model.
Genetics of Endocrine Disorders and Diabetes Mellitus
Published in George H. Gass, Harold M. Kaplan, Handbook of Endocrinology, 2020
Bess Adkins Marshall, Abby Solomon Hollander
MEN1 patients manifest tumors of the anterior pituitary, the parathyroid glands, and the pancreatic islets. Adrenocortical and thyroid tumors are occasionally associated with the syndrome.1 The disorder is inherited in an autosomal dominant manner. The MEN1 gene has been mapped to chromosome 11q13 by linkage analysis.2 Two recent papers propose two different genes in the area of the chromosome linked to the syndrome. The first proposes a gene termed ZFM1 (for zinc finger gene in the MEN1 locus). The nucleotide sequence of the clone predicts a gene containing 14 exons and 623 amino acids, part of which appears to be a metal-binding domain (zinc finger motif), which is seen in nucleic acid-binding proteins. The putative protein has some similarity to the Wilms’ tumor gene product and the early growth response 2 protein.3 The other proposed gene is nearby on chromosome 11q13 and was located using deletion mapping of parathyroid tumors. This gene codes for a previously described protein, phospholipase C β3 (PLC β3), which, based on the activity of similar proteins, may be involved in signal transduction, intracellular calcium regulation, or activation of protein kinase C, which are in turn involved in cell growth and differentiation.4 There are no studies to date showing specific defects in either of these genes that cosegregate with MEN1 syndrome in affected families, so it is not yet clear which, if either, of these genes is responsible for the syndrome.
Learning about quantitative genetics from Marla Sokolowski
Published in Journal of Neurogenetics, 2021
Localizing genes for quantitative traits by conventional recombination mapping is always a formidable challenge because environmental variation, minor genes, and genetic markers have modifying effects on continuously varying phenotypes such as foraging. To compensate for this, de Belle and colleagues used ‘lethal tagging’ and deletion mapping to localize the gene to the left arm of chromosome 2. This involved generating radiation-induced lethal alleles that would fail to complement the recessive sitter phenotype. The result provided a salivary-chromosome-band level of resolution. The last necessary link came from seeing in the literature that the structural locus for one of the two cGMP-dependent protein kinases in Drosophila (dg2) mapped to the same salivary chromosome band (Kalderon & Rubin, 1989) as foraging.
Importin-α2 mediates brain development, learning and memory consolidation in Drosophila
Published in Journal of Neurogenetics, 2020
Christine N. Serway, Brian S. Dunkelberger, Denise Del Padre, Nicole W. C. Nolan, Stephanie Georges, Stephanie Freer, Andrew J. Andres, J. Steven de Belle
At the time we initiated this study, crude recombination data based on the mbmB brain histology phenotype indicated a position at 2–31 on the left arm of chromosome-2 (Heisenberg et al., 1985). Since mbmB females were observed to be sterile (de Belle & Heisenberg, 1996; Ginsburg, 2002) we leveraged this more expedient phenotype in further analyses (Figure S3(A)). A comprehensive deletion mapping experiment (>165 deletions/mbmB scored for female sterility) revealed that Df(2L)BSC50 (BSC50) failed to complement mbmB: all transheterozygous females were sterile with small MBs (Figure 2(A,B); see Supplementary Figure S3(B) for details). Overlapping deficiencies complimenting mbmB restricted our map designation to 30F4-6. Sequencing in this region identified a G-to-A transition in codon #262 of Pen, encoding Imp-α2 (hereafter referred to as imp-α2; Figure 2(A)). This nonsense mutation leading to a premature stop codon in place of wild-type tryptophan was expected to generate a truncated Imp-α2 protein. Of 25 tested P-elements in this region, we identified PBacPenc05212 (c05212) that failed to complement mbmB. We also found that imp-α2D14 (D14), an established null allele (Török et al., 1995) was female sterile, had strongly reduced MBs and similarly did not complement mbmB (Figure 2(B)).
The Drosophila melanogaster foraging gene affects social networks
Published in Journal of Neurogenetics, 2021
Nawar Alwash, Aaron M. Allen, Marla B. Sokolowski, Joel D. Levine
Quantitative genetic analysis of the rover-sitter difference in larval foraging path-length supported a primarily Mendelian model of an autosomal gene with the rover phenotype (long path-length phenotype) exhibiting complete genetic dominance to the sitter (short path-length phenotype) (de Belle & Sokolowski, 1987). The mapping of an autosomal gene responsible for rover-sitter differences showed that it mapped to the left arm of chromosome-2 (de Belle & Sokolowski, 1989). To more precisely map the larval path-length phenotype de Belle, Hilliker, & Sokolowski (1989) developed the lethal tagging technique. Lethal tagging involved mutagenesis of the rover strain, crossing it to the sitter strain, and screening for sitter behaving larvae that carry a recessive lethal allele that tagged the gene responsible for rover-sitter differences in foraging path-length. Five alleles of the gene named foraging (for) were identified, all of which failed to complement for foraging path-length behavior (de Belle et al., 1989). Three of these five lines also failed to complement the pupal lethality and identified the lethal tag of the gene. The other two lines carried viable sitter alleles. Recombination and deletion mapping localized the rover-sitter foraging path-length difference to cytological region 24A3-5 (see also de Belle et al., 1989, de Belle, Sokolowski, & Hilliker, 1993). To further localize the gene, de Belle et al. (1993) generated a complementation map of the region by inducing additional mutants in the rover strain and mapping the lethality and behavioral alteration (from rover to sitter) to within the 5′ end of the dg2 gene which encodes cGMP-dependent protein kinase (de Belle et al., 1989, 1993; de Belle & Sokolowski, 1987, 1989; Kalderon & Rubin, 1989). Molecular analyses further demonstrated that for is synonymous with dg2. for null alleles carrying a full deletion of the 35 kb genomic region of for are pupal lethal (Allen, Anreiter, Neville, & Sokolowski, 2017; Anreiter et al., 2021). The for null was rescued with a full genomic fragment of for/dg2 (Allen et al., 2017), and increasing for/dg2 with for-cDNA in a sitter resulted in rover larval path-lengths and higher PKG enzyme activities characteristic of rover confirming that for is dg2 (Allen et al., 2017; Osborne et al., 1997). Further research confirmed that for encodes a cGMP-dependent protein kinase (PKG), and plays an important role in food-related behaviors more generally (Allen et al., 2017; Anreiter and Sokolowski, 2019; Osborne et al., 1997). The for based rover-sitter differences in larval path length are for the most part robust to changes in the genetic background whether on lab or field derived genetic backgrounds (Sokolowski et al., 1997).