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Improved white spruce (Picea glauca) genome assemblies and annotation of large gene families of conifer terpenoid and phenolic defense metabolism 下载免费PDF全文
René L. Warren Christopher I. Keeling Macaire Man Saint Yuen Anthony Raymond Greg A. Taylor Benjamin P. Vandervalk Hamid Mohamadi Daniel Paulino Readman Chiu Shaun D. Jackman Gordon Robertson Chen Yang Brian Boyle Margarete Hoffmann Detlef Weigel David R. Nelson Carol Ritland Nathalie Isabel Barry Jaquish Alvin Yanchuk Jean Bousquet Steven J. M. Jones John MacKay Inanc Birol Joerg Bohlmann 《The Plant journal : for cell and molecular biology》2015,83(2):189-212
946.
Xin Gong Jingxian Li Wei Shao Jianping Wu Hongwu Qian Ruobing Ren Peter Espenshade Nieng Yan 《Cell research》2015,25(4):401-411
The sterol regulatory element-binding protein (SREBP) and SREBP cleavage-activating protein (SCAP) are central players in the SREBP pathway, which control the cellular lipid homeostasis. SCAP binds to SREBP through their carboxyl (C) domains and escorts SREBP from the endoplasmic reticulum to the Golgi upon sterol depletion. A conserved pathway, with the homologues of SREBP and SCAP being Sre1 and Scp1, was identified in fission yeast Schizosaccharomyces pombe. Here we report the in vitro reconstitution of the complex between the C domains of Sre1 and Scp1 as well as the crystal structure of the WD40 domain of Scp1 at 2.1 Å resolution. The structure reveals an eight-bladed β-propeller that exhibits several distinctive features from a canonical WD40 repeat domain. Structural and biochemical characterization led to the identification of two Scp1 elements that are involved in Sre1 recognition, an Arg/Lys-enriched surface patch on the top face of the WD40 propeller and a 30-residue C-terminal tail. The structural and biochemical findings were corroborated by in vivo examinations. These studies serve as a framework for the mechanistic understanding and further functional characterization of the SREBP and SCAP proteins in fission yeast and higher organisms. 相似文献
947.
Evolutionary change in testes tissue composition among experimental populations of house mice 下载免费PDF全文
Renée C. Firman Francisco Garcia‐Gonzalez Evan Thyer Samantha Wheeler Zayaputeri Yamin Michael Yuan Leigh W. Simmons 《Evolution; international journal of organic evolution》2015,69(3):848-855
Theory assumes that postcopulatory sexual selection favors increased investment in testes size because greater numbers of sperm within the ejaculate increase the chance of success in sperm competition, and larger testes are able to produce more sperm. However, changes in the organization of the testes tissue may also affect sperm production rates. Indeed, recent comparative analyses suggest that sperm competition selects for greater proportions of sperm‐producing tissue within the testes. Here, we explicitly test this hypothesis using the powerful technique of experimental evolution. We allowed house mice (Mus domesticus) to evolve via monogamy or polygamy in six replicate populations across 24 generations. We then used histology and image analysis to quantify the proportion of sperm‐producing tissue (seminiferous tubules) within the testes of males. Our results show that males that had evolved with sperm competition had testes with a higher proportion of seminiferous tubules compared with males that had evolved under monogamy. Previously, it had been shown that males from the polygamous populations produced greater numbers of sperm in the absence of changes in testes size. We thus provide evidence that sperm competition selects for an increase in the density of sperm‐producing tissue, and consequently increased testicular efficiency. 相似文献
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Hsiuchen Chen Shuxun Ren Clary Clish Mohit Jain Vamsi Mootha J. Michael McCaffery David C. Chan 《The Journal of cell biology》2015,211(4):795-805
Defects in mitochondrial fusion or fission are associated with many pathologies, raising the hope that pharmacological manipulation of mitochondrial dynamics may have therapeutic benefit. This approach assumes that organ physiology can be restored by rebalancing mitochondrial dynamics, but this concept remains to be validated. We addressed this issue by analyzing mice deficient in Mff, a protein important for mitochondrial fission. Mff mutant mice die at 13 wk as a result of severe dilated cardiomyopathy leading to heart failure. Mutant tissue showed reduced mitochondrial density and respiratory chain activity along with increased mitophagy. Remarkably, concomitant deletion of the mitochondrial fusion gene Mfn1 completely rescued heart dysfunction, life span, and respiratory chain function. Our results show for the first time that retuning the balance of mitochondrial fusion and fission can restore tissue integrity and mitochondrial physiology at the whole-organ level. Examination of liver, testis, and cerebellum suggest, however, that the precise balance point of fusion and fission is cell type specific. 相似文献