Sex and PRNP Genotype Determination in Preimplantation Caprine Embryos

2010 ◽  
Vol 46 (4) ◽  
pp. 656-663 ◽  
Author(s):  
F Guignot ◽  
C Perreau ◽  
C Cavarroc ◽  
J-L Touzé ◽  
J-L Pougnard ◽  
...  
Keyword(s):  
2009 ◽  
Vol 21 (3) ◽  
pp. 295-305 ◽  
Author(s):  
David A. Schneider ◽  
Ahmed Tibary ◽  
Terje Raudsepp ◽  
Pranab J. Das ◽  
Katherine I. O'Rourke

Classical scrapie disease is a transmissible spongiform encephalopathy of sheep that is enzootic in the United States. Susceptibility of sheep to classical scrapie is linked to single nucleotide polymorphisms in the prion protein gene ( PRNP), forming the basis for genetic testing strategies used by national efforts to eradicate scrapie. Such efforts are occasionally hampered by inconclusive results stemming from the detection of “complex” genotypes. Naturally occurring cases of ovine chimerism are thought to account for some of these instances. In the current report, 4 naturally occurring ovine chimeras are documented through cytogenetic and molecular analyses. All 4 of these sheep had chimeric cells circulating in their blood. Blood and alternate tissue samples of ear punch and hair bulbs from one of these chimeras was submitted in batch with similar samples from control sheep for routine scrapie genetic relative susceptibility testing. A complex PRNP genotype was detected in the blood of the chimeric female but not in the alternate tissue samples or in the control sheep samples. The results demonstrate that naturally occurring blood chimerism can confound current testing efforts. The potential impacts of undetected chimeras on current scrapie eradication efforts are discussed.


2018 ◽  
Vol 49 (1) ◽  
Author(s):  
Paola Sacchi ◽  
Roberto Rasero ◽  
Giuseppe Ru ◽  
Eleonora Aiassa ◽  
Silvia Colussi ◽  
...  

2010 ◽  
Vol 91 (10) ◽  
pp. 2630-2641 ◽  
Author(s):  
L. Gonzalez ◽  
S. Siso ◽  
E. Monleon ◽  
C. Casalone ◽  
L. J. M. van Keulen ◽  
...  

2006 ◽  
Vol 87 (4) ◽  
pp. 1043-1046 ◽  
Author(s):  
Olivier Andréoletti ◽  
Nathalie Morel ◽  
Caroline Lacroux ◽  
Virginie Rouillon ◽  
Céline Barc ◽  
...  

Oral contamination with bovine spongiform encephalopathy (BSE) agent in susceptible PRNP genotype sheep results in widespread distribution of prion in the host. Because ARR homozygous sheep are considered to be resistant to transmissible spongiform encephalopathies, they have been selected to eradicate scrapie from sheep flocks and to protect the human food chain from small ruminant BSE risk. However, results presented here show that several months after an oral challenge with BSE agent, healthy ARR/ARR sheep can accumulate significant amounts of PrPSc in the spleen.


2012 ◽  
Vol 43 (1) ◽  
pp. 55 ◽  
Author(s):  
Lorenzo González ◽  
Martin Jeffrey ◽  
Mark P Dagleish ◽  
Wilfred Goldmann ◽  
Sílvia Sisó ◽  
...  

Genetics ◽  
2003 ◽  
Vol 165 (4) ◽  
pp. 2085-2091 ◽  
Author(s):  
Carole R Moreno ◽  
Frédéric Lantier ◽  
Isabelle Lantier ◽  
Pierre Sarradin ◽  
Jean-Michel Elsen

AbstractSusceptibility to scrapie is largely controlled by the PRNP gene in mice and in several other species. However, individuals with identical scrapie susceptibility Prnp alleles may have very different incubation periods, suggesting the influence of other environmental and genetic factors. To detect loci influencing susceptibility to TSE, two mouse lines carrying the same PRNP genotype (C57BL and RIII) were crossed to produce an F2 population inoculated intracerebrally with a mouse-adapted scrapie strain. Linkage was studied between 72 markers and the age of death of F2 animals. Six QTL were detected, two at a genome-wide significant level (chromosomes 5 and 7) and four at a genome-wide suggestive level (chromosomes 4, 6, 8, and 17). Our results confirmed the existence of some QTL that were detected previously (chromosomes 4, 6, 7, and 8) while others were found only in the present study (chromosomes 5 and 17). Furthermore, it seems that some QTL (chromosomes 4 and 8) are involved in resistance to scrapie as well as to BSE.


2014 ◽  
Vol 50 (3) ◽  
pp. 660-665 ◽  
Author(s):  
Lisa L. Wolfe ◽  
Karen A. Fox ◽  
Michael W. Miller

2017 ◽  
Vol 214 (12) ◽  
pp. 3481-3495 ◽  
Author(s):  
Zuzana Krejciova ◽  
James Alibhai ◽  
Chen Zhao ◽  
Robert Krencik ◽  
Nina M. Rzechorzek ◽  
...  

Prions are infectious agents that cause neurodegenerative diseases such as Creutzfeldt–Jakob disease (CJD). The absence of a human cell culture model that replicates human prions has hampered prion disease research for decades. In this paper, we show that astrocytes derived from human induced pluripotent stem cells (iPSCs) support the replication of prions from brain samples of CJD patients. For experimental exposure of astrocytes to variant CJD (vCJD), the kinetics of prion replication occur in a prion protein codon 129 genotype–dependent manner, reflecting the genotype-dependent susceptibility to clinical vCJD found in patients. Furthermore, iPSC-derived astrocytes can replicate prions associated with the major sporadic CJD strains found in human patients. Lastly, we demonstrate the subpassage of prions from infected to naive astrocyte cultures, indicating the generation of prion infectivity in vitro. Our study addresses a long-standing gap in the repertoire of human prion disease research, providing a new in vitro system for accelerated mechanistic studies and drug discovery.


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