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Luca Nguyen
Luca Nguyen

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The sequences of miRNAs predicted in Alexandrium tamarense were similar to those of certain human or mouse miRNAs, although the seed miRNAs used for homologous searches were taken from both plant and animal species (Table 1). This finding can be explained by observations from previous studies that have found that most diatom miRNAs share similarities with those of animals.21 Because diatoms have a mosaic genome that contain genes from animals, plants, and bacteria, it is speculated that these animal-like miRNAs may have been introduced in diatoms via gene transformation and endosymbiosis during evolution.41 Like the genome of diatoms, the genome of dinoflagellates has also been dramatically influenced by small- and large-scale lateral transfer through serial endosymbiosis.25 Thus, we deduced that the 18 putative miRNAs of Alexandrium tamarense may have originated through lateral or horizontal gene transfer during the early stages of its evolution.




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Western blot analysis of proteinase-K resistant L-BSE PrPSc in TgBoPrP mice before and after passage in sheep. The brain samples of TgBoPrP mice inoculated intracerebrally with either L-BSE/cattle or L-BSE/sheep were analyzed. PrPSc in the twice-passaged mice was detected with mAb T2. The numbers indicate three different mice.


To the best of our knowledge, the transmission of L-BSE/cattle to wild-type mice has only been reported in one study, and even in this case the L-BSE prions were converted to a C-BSE-like prion using serial passages, and had indistinguishable phenotypic traits compared with mouse-passaged C-BSE [17]. A phenotypic change during the transmission of prions is a common phenomenon across a species barrier [33,38,39]. However, the reasons for the discrepancy between this study here and another, suggesting that BASE prion converts into C-BSE-like phenotypes during interspecies transmission in wild-type mice [17] are unknown. Several possible reasons are concisely considered: (1) cross contamination may occur during the inoculation procedure, (2) undetectable levels of C-BSE agent by WB analysis emerge in the brain of mice challenged with BASE at the first passage, thereafter inoculated mice develop the disease in subsequent passages [29], (3) L-BSE could generate at least 2 types of prions in wild-type mice: one showing L-BSE phenotypic properties and the other producing C-BSE-like signatures, (4) differences of unidentified prion-related host factors between outbred (ICR) and inbred (C57BL/6, SJL, or RIII) mice may have influenced the emergence of C-BSE-like prions during the cross-species transmission, and (5) differences of experimental procedures including prepared inocula and/or challenge routes of the infection may have influenced the propagation and/or generation of PrPSc in the brain. The first two possibilities were completely ruled out by the authors [17]. The last possibility, is that mice were inoculated by a combination of intracerebral and intraperitoneal routes with a thalamic sample at first passage and with brain pools prepared from C57Bl/6 or SJL mice at second passage [17], should help address this issue [40]. No transmissibility including lymphotropism was found on the first passage in the Italian study. Although PrPSc was undetectable in the brain of these mice, a faint positive signal was identified in one RIII mouse that showed biochemical characteristics of PrPSc identical to those of C-BSE-infected mice by WB analyses.


Panel showing serial sections taken from the frontal lobe of cattle infected withH-BSE. Sections were immunolabeled with three mAbs (P4, 12F10 and F99/97.6.1), detectedusing the TSA-biotin system and counterstained with HE. The upper row indicates a lowmagnification image of the frontal lobe. Immunolabeled PrPSc accumulatedwidely in the cerebral gray matter (left side), but less in the white matter (rightside). The middle row shows a high-magnification image of the frontal gray matter. Thebottom row shows a high-magnification image of the frontal white matter.


Comparison of PrPSc immunolabeling intensity on serial sections oftrigeminal ganglion, adrenal medulla, optic nerve and retina using three different mAbs(P4, 12F10 and F99/97.6.1), detected with the TSA-biotin system and counterstained withHE. MAb F99/97.6.1 resulted in the most intense labeling (bottom row). Only faintimmunoreactivity was observed within the glial cells of the optic nerve (arrows), but noPrPSc deposits were observed in the trigeminal ganglion, adrenal and retinausing mAb P4. Abbreviations in the Retina column: NFL, nerve fiber layer; GCL, ganglioncell layer; IPL, inner plexiform layer; INL, inner nucleus layer; OPL, outer plexiformlayer; ONL, outer nucleus layer; OS, outer segments. 350c69d7ab


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