A quasi-exclusive European ancestry in the Senepol tropical cattle breed highlights the importance of the slick locus in tropical adaptation.

BACKGROUND: The Senepol cattle breed (SEN) was created in the early XX(th) century from a presumed cross between a European (EUT) breed (Red Poll) and a West African taurine (AFT) breed (N'Dama). Well adapted to tropical conditions, it is also believed trypanotolerant according to its putative AFT ancestry. However, such origins needed to be verified to define relevant husbandry practices and the genetic background underlying such adaptation needed to be characterized. METHODOLOGY/PRINCIPAL FINDINGS: We genotyped 153 SEN individuals on 47,365 SNPs and combined the resulting data with those available on 18 other populations representative of EUT, AFT and Zebu (ZEB) cattle. We found on average 89% EUT, 10.4% ZEB and 0.6% AFT ancestries in the SEN genome. We further looked for footprints of recent selection using standard tests based on the extent of haplotype homozygosity. We underlined i) three footprints on chromosome (BTA) 01, two of which are within or close to the polled locus underlying the absence of horns and ii) one footprint on BTA20 within the slick hair coat locus, involved in thermotolerance. Annotation of these regions allowed us to propose three candidate genes to explain the observed signals (TIAM1, GRIK1 and RAI14). CONCLUSIONS/SIGNIFICANCE: Our results do not support the accepted concept about the AFT origin of SEN breed. Initial AFT ancestry (if any) might have been counter-selected in early generations due to breeding objectives oriented in particular toward meat production and hornless phenotype. Therefore, SEN animals are likely susceptible to African trypanosomes which questions the importation of SEN within the West African tsetse belt, as promoted by some breeding societies. Besides, our results revealed that SEN breed is predominantly a EUT breed well adapted to tropical conditions and confirmed the importance in thermotolerance of the slick locus.

Ultraestructura renal en infecciones murinas experimentales con un aislado venezolano de Trypanosoma evansi / Renal ultrastructure in experimental murine infections with a Venezuelan isolate of Trypanosoma evansi

Infecciones murinas experimentales con un aislado venezolano de Trypanosoma evansi ocasionan cambios ma - cros copicos y ultraestructurales en el rinon de los ratones. La modificacion macroscopica se restringe a palidez progresiva del organo. Por su parte, las alteraciones ultraestructurales incluyen incremento del grosor de la membrana basal glomerular, asi como del espesor de la membrana basal de los tubulos contorneados proximales, cambios en la colocacion y el agrupamiento de las mitocondrias asociadas a la lamina basal, asi como extenso deterioro epitelial. Los tripanosomas intravasculares fueron detectados en la circulacion renal a partir de dia 9 post-infeccion. Se discute al respecto del dano glomerular, sugiriendo que las alteraciones submicroscopicas debilitarian la funcion tubular, contribuyendo mediante un proceso nefritico al desarrollo de una falla renal aguda que culminaria con la muerte del hospedador experimental. La significancia de los cambios ultraestructurales fue corroborada estadisticamente.

Murine experimental inoculations with a Venezuelan isolate of Trypanosoma evansi cause macroscopic and ultrastructural changes in the kidney of the infected animals. The macroscopic modifications are restricted to the progressive paleness of the organ. By its part, the ultrastructural alterations include thickness enlargement of the glomerular basal and the proximal tubule basal membranes, changes in the mitochondrial grouping and layout close to the basal membrane, as well as extensive epithelial damage. Intra vascu - lar trypanosomes were seen in the renal circulation from day 9 post-infection and on. The glomerular injury is discussed, suggesting that submicroscopic alterations could weaken the tubular function contributing through a nephritic process with the development of an acute renal failure culminating in the experimental host¡¦s death. The significance of the sequential increasing ultrastructural changes was statistically corroborated.