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Mobile DNA Sequences and Their Possible Role in Evolution
Published in S. K. Dutta, DNA Systematics, 2019
Georgii P. Georgiev, Yurii V. Ilyin, Alexei P. Ryskov, Tatiana I. Gerasimova
Possibly there are elements in the genome other than P-elements which can also encode “transposase”. Being expressed, such elements might induce the excision-insertion of sequences with appropriate organization of the termini.
The Concept of Health
Published in Dien Ho, A Philosopher Goes to the Doctor, 2019
One fascinating question is how nasty genes could find a stable home in a genome. Wouldn’t the deleterious effects of these genes on their hosts be akin to burning down one’s house? How could they stick around for so long if they are bad for their host’s survival? One possible answer is that whatever negative effects they might have on our reproductive fitness, they make up for them in their superior abilities to pass themselves onto future generations. In other words, the host might have a shorter and more reproductively challenged life, but if the genes can make up for the shorter window with a greater number of offspring, these nasty genes are still ahead of the evolutionary curve. In a study of Drosophila melanogaster (or common fruit flies), Struchiner, Kidwell, and Ribeiro (2005) found just such an example. They discovered that a specific transposon (P elements) lowers the reproductive fitness of fruit flies by 19%. Like any genetic traits, there is a 50% chance that a given one is present in a specific gamete. Struchiner et al. noticed instead that P elements are present in 70% of the gametes, which means the transposon is able to increase its odds of being passed on. Even though the presence of P elements lowers the host’s reproductive fitness, the 20% increased odds of their presence in gametes outweighs the cost to the host. As such, it reaches a stable place among the genomes of generations of fruit flies by rendering these flies less reproductive while making sure that it is more likely to be in a gamete. In essence, the transposon behaves much like a permanent parasite: stringing the host along and making it less fit, all the while looking out for its own agenda.8
Generation and characterization of fruitless P1 promoter mutant in Drosophila melanogaster
Published in Journal of Neurogenetics, 2021
Megan C. Neville, Alexander Eastwood, Aaron M. Allen, Ammerins de Haan, Tetsuya Nojima, Stephen F. Goodwin
Fast forward 20 years, the Wasserman lab, looking for single P-element insertion mutants which cause male sterility, again identified mutations which caused males to court other males, and mapped to the fru locus (Castrillon et al., 1993). These new alleles of fru (fru3 and fru4) made it possible to clone the gene through complementation analysis of mapped deficiencies with these alleles, followed by a chromosomal walk (Ryner et al., 1996). A contemporary P-element insertion screen, in the Yamamoto lab, focused on identifying behaviorally sterile males, uncovered a different allele of fru (frusat) which enabled concurrent cloning of the fru gene (Ito et al., 1996). Collectively these studies unearthed the molecular secrets of the gene, characterizing fru DNA and mRNA sequences and determined that it encoded a member of the BTB-Zn-finger family of transcriptional regulators (Siggs & Beutler, 2012). This new collection of fru alleles contributed to our initial understanding of how fru regulated courtship from the behavioral analysis of males and females carrying mutations at the locus (Villella et al., 1997).
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)).
Update on: proteome analysis in thyroid pathology – part II: overview of technical and clinical enhancement of proteomic investigation of the thyroid lesions
Published in Expert Review of Proteomics, 2018
Isabella Piga, Stefano Casano, Andrew Smith, Silvia Tettamanti, Davide Leni, Giulia Capitoli, Angela Ida Pincelli, Marcella Scardilli, Stefania Galimberti, Fulvio Magni, Fabio Pagni
IHC applications are useful not only in preoperative FNA but also in formalin-fixed paraffin- embedded tissue (FFPE) surgical tissues. Pathologists may encounter diagnostic challenges in histopathology, since the definition of morphological (nuclear and architectural) criteria is not always reproducible and standardized. In this sense, ancillary IHC stainings should improve the diagnostic performances, highlighting specific tissue antigens. The Ki-67 proliferation index was studied, but with conflicting results regarding a positive cut-off value of its nuclear expression [10]. P-element induced wimpy testis like 2 (PIWIL2) may become a marker for the diagnosis and prognosis of PTC whilst also being a potential therapeutic target in the future [17]. In fact, PIWIL2 was present in 95.6% of tumoral tissue and 8.9% of non-tumoral tissues (p < 0.01), both as a protein itself and as mRNA, thus suggesting a possible key role in the formation and progression of thyroid cancer.