scholarly journals Testing the importance of harvest refuges for phenotypic rescue of trophy‐hunted populations

2020 ◽  
Vol 57 (3) ◽  
pp. 526-535
Author(s):  
Yoanna Poisson ◽  
Marco Festa‐Bianchet ◽  
Fanie Pelletier
Keyword(s):  
Phenotypic Rescue

scholarly journals The Functions of the Multiproduct and Rapidly Evolving dec-1 Eggshell Gene Are Conserved Between Evolutionarily Distant Species of Drosophila

Genetics ◽  
2001 ◽  
Vol 159 (3) ◽  
pp. 1089-1102
Author(s):  
James C Badciong ◽  
Jeffery M Otto ◽  
Gail L Waring
Keyword(s):  
Biological Significance ◽  
Extracellular Proteins ◽  
Female Fertility ◽  
Open Reading Frames ◽  
Amino Acid Variability ◽  
Normal Expression ◽  
Evolutionary Comparison ◽  
Phenotypic Rescue ◽  
Conserved Amino Acids ◽  
Reading Frames

Abstract The Drosophila dec-1 gene encodes multiple proteins that are required for female fertility and proper eggshell morphogenesis. Genetic and immunolocalization data suggest that the different DEC-1 proteins are functionally distinct. To identify regions within the proteins with potential biological significance, we cloned and sequenced the D. yakuba and D. virilis dec-1 homologs. Interspecies comparisons of the predicted translation products revealed rapidly evolving sequences punctuated by blocks of conserved amino acids. Despite extensive amino acid variability, the proteins produced by the different dec-1 homologs were functionally interchangeable. The introduction of transgenes containing either the D. yakuba or the D. virilis dec-1 open reading frames into a D. melanogaster DEC-1 protein null mutant was sufficient to restore female fertility and wild-type eggshell morphology. Normal expression and extracellular processing of the DEC-1 proteins was correlated with the phenotypic rescue. The nature of the conserved features highlighted by the evolutionary comparison and the molecular resemblance of some of these features to those found in other extracellular proteins suggests functional correlates for some of the multiple DEC-1 derivatives.

PHENOTYPIC RESCUE IN A MOUSE MODEL OF TAUOPATHY BY EARLY MODULATION OF TAU ISOFORMS’ RELATIVE CONTENT

2017 ◽  
Vol 13 (7) ◽  
pp. P205
Author(s):  
Sonia Espindola ◽  
Ana Damianich ◽  
Manuela Sartor ◽  
Juan Belforte ◽  
Jean-Marc Gallo ◽  
...  
Keyword(s):  
Mouse Model ◽  
Relative Content ◽  
Tau Isoforms ◽  
Phenotypic Rescue

Phenotypic rescue of mutant brown melanocytes by a retrovirus carrying a wild-type tyrosinase-related protein gene

Development ◽  
1990 ◽  
Vol 110 (2) ◽  
pp. 471-475 ◽  
Author(s):  
D.C. Bennett ◽  
D. Huszar ◽  
P.J. Laipis ◽  
R. Jaenisch ◽  
I.J. Jackson
Keyword(s):  
Coat Colour ◽  
Specific Protein ◽  
Related Protein ◽  
Histone H4 ◽  
Wild Type ◽  
Leukaemia Virus ◽  
Mouse Cdna ◽  
Phenotypic Rescue ◽  
Moloney Murine Leukaemia Virus ◽  
Tyrosinase Related Protein

A mouse cDNA for the developmentally controlled, melanocyte-specific protein, tyrosinase-related protein 1 (TRP-1), was previously cloned and reported to show genetic linkage with the coat-colour locus brown (b) on mouse chromosome 4. The cDNA has been inserted into a retroviral vector derived from Moloney murine leukaemia virus, under the control of the human histone H4 promoter. This vector was used to infect melanocytes of the immortal line melan-b, which are homozygous for the b mutation and which display light brown pigmentation in culture. Infected cultures containing between 0.2 and 2 copies of provirus per cell displayed an altered phenotype: 20–50% of cells now had the black to dark brown colour characteristic of cultured wild-type (Black, B/B) mouse melanocytes. Thus the TRP-1 gene complements the brown mutation. We conclude that TRP-1 is the product of the wild-type b-locus.

scholarly journals Phenotypic rescue of a Drosophila model of mitochondrial ANT1 disease

2014 ◽  
Vol 7 (6) ◽  
pp. 635-648 ◽  
Author(s):  
S. Vartiainen ◽  
S. Chen ◽  
J. George ◽  
T. Tuomela ◽  
K. R. Luoto ◽  
...  
Keyword(s):  
Drosophila Model ◽  
Phenotypic Rescue

scholarly journals Specific Myosin Heavy Chain Mutations Suppress Troponin I Defects in Drosophila Muscles

1999 ◽  
Vol 144 (5) ◽  
pp. 989-1000 ◽  
Author(s):  
William A. Kronert ◽  
Angel Acebes ◽  
Alberto Ferrús ◽  
Sanford I. Bernstein
Keyword(s):  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Thin Filament ◽  
Troponin I ◽  
Point Mutations ◽  
Thick Filament ◽  
Actin Binding ◽  
Filament Protein ◽  
Phenotypic Rescue

We show that specific mutations in the head of the thick filament molecule myosin heavy chain prevent a degenerative muscle syndrome resulting from the hdp2 mutation in the thin filament protein troponin I. One mutation deletes eight residues from the actin binding loop of myosin, while a second affects a residue at the base of this loop. Two other mutations affect amino acids near the site of nucleotide entry and exit in the motor domain. We document the degree of phenotypic rescue each suppressor permits and show that other point mutations in myosin, as well as null mutations, fail to suppress the hdp2 phenotype. We discuss mechanisms by which the hdp2 phenotypes are suppressed and conclude that the specific residues we identified in myosin are important in regulating thick and thin filament interactions. This in vivo approach to dissecting the contractile cycle defines novel molecular processes that may be difficult to uncover by biochemical and structural analysis. Our study illustrates how expression of genetic defects are dependent upon genetic background, and therefore could have implications for understanding gene interactions in human disease.

scholarly journals Precise Deletion of tagD and Controlled Depletion of Its Product, Glycerol 3-Phosphate Cytidylyltransferase, Leads to Irregular Morphology and Lysis of Bacillus subtilisGrown at Physiological Temperature

2001 ◽  
Vol 183 (22) ◽  
pp. 6688-6693 ◽  
Author(s):  
Amit P. Bhavsar ◽  
Terry J. Beveridge ◽  
Eric D. Brown
Keyword(s):  
Bacillus Subtilis ◽  
Gene Product ◽  
Genetic Background ◽  
Expression System ◽  
Teichoic Acid ◽  
Structural Defects ◽  
Acid Biosynthesis ◽  
Physiological Temperature ◽  
Conditional Expression ◽  
Phenotypic Rescue

ABSTRACT Using a previously reported conditional expression system for use in Bacillus subtilis (A. P. Bhavsar, X. Zhao, and E. D. Brown, Appl. Environ. Microbiol. 67:403–410, 2001), we report the first precise deletion of a teichoic acid biosynthesis (tag) gene, tagD,in B. subtilis. This teichoic acid mutant showed a lethal phenotype when characterized at a physiological temperature and in a defined genetic background. This tagD mutant was subject to full phenotypic rescue upon expression of the complementing copy oftagD. Depletion of the tagD gene product (glycerol 3-phosphate cytidylyltransferase) via modulated expression of tagD from the amyE locus revealed structural defects centered on shape, septation, and division. Thickening of the wall and ultimately lysis followed these events.

scholarly journals Can phenotypic rescue from harvest refuges buffer wild sheep from selective hunting?

2014 ◽  
Vol 4 (17) ◽  
pp. 3375-3382 ◽  
Author(s):  
Fanie Pelletier ◽  
Marco Festa‐Bianchet ◽  
Jon T. Jorgenson ◽  
Chiarastella Feder ◽  
Anne Hubbs
Keyword(s):  
Wild Sheep ◽  
Phenotypic Rescue

scholarly journals A phenotypic rescue approach identifies lineage regionalization defects in a mouse model of DiGeorge syndrome

2021 ◽  
Author(s):  
Gabriella Lania ◽  
Monica Franzese ◽  
Adachi Noritaka ◽  
Marchesa Bilio ◽  
Annalaura Russo ◽  
...  
Keyword(s):  
Mouse Model ◽  
Vitamin B12 ◽  
Aortic Arch ◽  
Digeorge Syndrome ◽  
Molecular Level ◽  
Cellular Distribution ◽  
Cell Distribution ◽  
Pharyngeal Apparatus ◽  
Phenotypic Rescue

ABSTRACTTBX1 is a key regulator of pharyngeal apparatus (PhAp) development. Vitamin B12 treatment partially rescues aortic arch patterning defects of Tbx1+/- embryos. Here we show that it also improves cardiac outflow tract septation and branchiomeric muscle anomalies of Tbx1 hypomorphic mutants. At molecular level, the in vivo vB12 treatment let us to identify genes that were dysregulated by Tbx1 haploinsufficiency and rescued by treatment. We found that SLUG, encoded by the rescued gene Snai2, identified a population of mesodermal cells that was partially overlapping with but distinct from ISL1+ and TBX1+ populations. In addition, SLUG+ cells were mislocalized and had a greater tendency to aggregate in Tbx1+/- and Tbx1-/- embryos and vB12 treatment restore cellular distribution. Adjacent neural crest-derived mesenchymal cells, which do not express TBX1, were also affected, showing enhanced segregation from cardiopharyngeal mesodermal cells. We propose that TBX1 regulates cell distribution in core mesoderm and the arrangement of multiple lineages within the PhAp.

Molecular cloning of fused, a gene required for normal segmentation in the Drosophila melanogaster embryo

1987 ◽  
Vol 7 (9) ◽  
pp. 3244-3251
Author(s):  
M C Mariol ◽  
T Preat ◽  
B Limbourg-Bouchon
Keyword(s):  
Drosophila Melanogaster ◽  
Genomic Dna ◽  
Developmental Stages ◽  
Developmental Expression ◽  
Segment Polarity ◽  
D Region ◽  
Fused Gene ◽  
Phenotypic Rescue ◽  
Segment Polarity Gene ◽  
Polarity Gene

Using the chromosomal walk technique, we isolated recombinant lambda bacteriophage and cosmid clones spanning 250 kilobases (kb) in the 17C-D region of the X chromosome of Drosophila melanogaster. This region was known to contain the segment polarity gene fused. Several lethal fused mutations were used to define more precisely the localization of this locus. Southern analysis of genomic DNA revealed that all of them were relatively large deficiencies, the smallest one being 40 kb long. None of the 12 viable fused mutations examined possessed detectable alterations. We isolated a cosmid containing an insertion covering the entire smallest fused deletion (40 kb). We injected this DNA into fused mutant embryos and obtained a partial phenotypic rescue of the embryonic pattern, indicating that this region contained all the sequences necessary for the embryonic expression of the fu+ gene. Within this DNA, a subclone of 14 kb codes for poly(A)+ RNAs of 3.5, 2.5, 1.6, and 1.3 kb detected in embryos from various developmental stages as well as in adults. All these transcripts showed the same developmental expression. This transcribed region was injected into fused mutant embryos, and once again we obtained a partial rescue of the embryonic phenotype, confirming that this region contained at least the fused gene.

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