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mtDNA diversity in rhesus monkeys reveals overestimates of divergence time and paraphyly with neighboring species 总被引:4,自引:0,他引:4
Reconstructions of the human-African great ape phylogeny by using
mitochondrial DNA (mtDNA) have been subject to considerable debate. One
confounding factor may be the lack of data on intraspecific variation. To
test this hypothesis, we examined the effect of intraspecific mtDNA
diversity on the phylogenetic reconstruction of another Plio- Pleistocene
radiation of higher primates, the fascicularis group of macaque (Macaca)
monkey species. Fifteen endonucleases were used to identify 10 haplotypes
of 40-47 restriction sites in M. mulatta, which were compared with similar
data for the other members of this species group. Interpopulational,
intraspecific mtDNA diversity was large (0.5%- 4.5%), and estimates of
divergence time and branching order incorporating this variation were
substantially different from those based on single representatives of each
species. We conclude that intraspecific mtDNA diversity is substantial in
at least some primate species. Consequently, without prior information on
the extent of genetic diversity within a particular species, intraspecific
variation must be assessed and accounted for when reconstructing primate
phylogenies. Further, we question the reliability of hominoid mtDNA
phylogenies, based as they are on one or a few representatives of each
species, in an already depauperate superfamily of primates.
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F J Cubero A Singh E Borkham-Kamphorst Y A Nevzorova M Al Masaoudi U Haas M V Boekschoten N Gassler R Weiskirchen M Muller C Liedtke C Trautwein 《Cell death and differentiation》2013,20(11):1580-1592
Death receptor-mediated hepatocyte apoptosis is implicated in a wide range of liver diseases including viral and alcoholic hepatitis, ischemia/reperfusion injury, fulminant hepatic failure, cholestatic liver injury, as well as cancer. Deletion of NF-κB essential modulator in hepatocytes (IKKγ/Nemo) causes spontaneous progression of TNF-mediated chronic hepatitis to hepatocellular carcinoma (HCC). Thus, we analyzed the role of death receptors including TNFR1 and TRAIL in the regulation of cell death and the progression of liver injury in IKKγ/Nemo-deleted livers. We crossed hepatocyte-specific IKKγ/Nemo knockout mice (NemoΔhepa) with constitutive TNFR1−/− and TRAIL−/− mice. Deletion of TNFR1, but not TRAIL, decreased apoptotic cell death, compensatory proliferation, liver fibrogenesis, infiltration of immune cells as well as pro-inflammatory cytokines, and indicators of tumor growth during the progression of chronic liver injury. These events were associated with diminished JNK activation. In contrast, deletion of TNFR1 in bone-marrow-derived cells promoted chronic liver injury. Our data demonstrate that TNF- and not TRAIL signaling determines the progression of IKKγ/Nemo-dependent chronic hepatitis. Additionally, we show that TNFR1 in hepatocytes and immune cells have different roles in chronic liver injury–a finding that has direct implications for treating chronic liver disease. 相似文献
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Plasticity of lifelong calorie‐restricted C57BL/6J mice in adapting to a medium‐fat diet intervention at old age 下载免费PDF全文
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Michela Baccini Eva-Maria Bachmaier Annibale Biggeri Mark V. Boekschoten Freek G. Bouwman Lorraine Brennan Robert Caesar Saverio Cinti Susan L. Coort Katie Crosley Hannelore Daniel Christian A. Drevon Susan Duthie Lars Eijssen Ruan M. Elliott Marjan van Erk Chris Evelo Mike Gibney Carolin Heim Graham W. Horgan Ian T. Johnson Thomas Kelder Robert Kleemann Teake Kooistra Martijn P. van Iersel Edwin C. Mariman Claus Mayer Gerard McLoughlin Michael Müller Francis Mulholland Ben van Ommen Abigael C. Polley Estelle Pujos-Guillot Isabel Rubio-Aliaga Helen M. Roche Baukje de Roos Manuela Sailer Giulia Tonini Lynda M. Williams Nicole de Wit 《Genes & nutrition》2008,3(3-4):147-151
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Robert Caesar Monia Manieri Thomas Kelder Mark Boekschoten Chris Evelo Michael Müller Teake Kooistra Saverio Cinti Robert Kleemann Christian A. Drevon 《PloS one》2010,5(7)
Depot-dependent differences in adipose tissue physiology may reflect specialized functions and local interactions between adipocytes and surrounding tissues. We combined time-resolved microarray analyses of mesenteric- (MWAT), subcutaneous- (SWAT) and epididymal adipose tissue (EWAT) during high-fat feeding of male transgenic ApoE3Leiden mice with histology, targeted lipidomics and biochemical analyses of metabolic pathways to identify differentially regulated processes and site-specific functions. EWAT was found to exhibit physiological zonation. De novo lipogenesis in fat proximal to epididymis was stably low, whereas de novo lipogenesis distal to epididymis and at other locations was down-regulated in response to high-fat diet. The contents of linoleic acid and α-linolenic acid in EWAT were increased compared to other depots. Expression of the androgen receptor (Ar) was higher in EWAT than in MWAT and SWAT. We suggest that Ar may mediate depot-dependent differences in de novo lipogenesis rate and propose that accumulation of linoleic acid and α-linolenic acid in EWAT is favored by testosterone-mediated inhibition of de novo lipogenesis and may promote further elongation and desaturation of these polyunsaturated fatty acids during spermatogenesis. 相似文献
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Domenico Sergi Fiona M. Campbell Christine Grant Amanda C. Morris Eva-Maria Bachmair Christiane Koch Fiona H. McLean Aifric Muller Nigel Hoggard Baukje de Roos Begona Porteiro Mark V. Boekschoten Fiona C. McGillicuddy Darcy Kahn Phyllis Nicol Jonas Benzler Claus-Dieter Mayer Janice E. Drew Helen M. Roche Michael Muller Ruben Nogueiras Carlos Dieguez Alexander Tups Lynda M. Williams 《Genes & nutrition》2018,13(1):28
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Jane L Wagstaff Jonathan N Pruneda Stefan MV Freund David Komander 《The EMBO journal》2017,36(24):3555-3572
The Ser/Thr protein kinase PINK1 phosphorylates the well‐folded, globular protein ubiquitin (Ub) at a relatively protected site, Ser65. We previously showed that Ser65 phosphorylation results in a conformational change in which Ub adopts a dynamic equilibrium between the known, common Ub conformation and a distinct, second conformation wherein the last β‐strand is retracted to extend the Ser65 loop and shorten the C‐terminal tail. We show using chemical exchange saturation transfer (CEST) nuclear magnetic resonance experiments that a similar, C‐terminally retracted (Ub‐CR) conformation also exists at low population in wild‐type Ub. Point mutations in the moving β5 and neighbouring β‐strands shift the Ub/Ub‐CR equilibrium. This enabled functional studies of the two states, and we show that while the Ub‐CR conformation is defective for conjugation, it demonstrates improved binding to PINK1 through its extended Ser65 loop, and is a superior PINK1 substrate. Together our data suggest that PINK1 utilises a lowly populated yet more suitable Ub‐CR conformation of Ub for efficient phosphorylation. Our findings could be relevant for many kinases that phosphorylate residues in folded protein domains. 相似文献
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