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1.
2.
For several species of lepidoptera, most of the approximately 350-bp
mitochondrial control-region sequences were determined. Six of these
species are in one genus, Jalmenus; are closely related; and are believed
to have undergone recent rapid speciation. Recent speciation was supported
by the observation of low interspecific sequence divergence. Thus, no
useful phylogeny could be constructed for the genus. Despite a surprising
conservation of control-region length, there was little conservation of
primary sequences either among the three lepidopteran genera or between
lepidoptera and Drosophila. Analysis of secondary structure indicated only
one possible feature in common--inferred stem loops with higher-than-random
folding energies-- although the positions of the structures in different
species were unrelated to regions of primary sequence similarity. We
suggest that the conserved, short length of control regions is related to
the observed lack of heteroplasmy in lepidopteran mitochondrial genomes. In
addition, determination of flanking sequences for one Jalmenus species
indicated (i) only weak support for the available model of insect 12S rRNA
structure and (ii) that tRNA translocation is a frequent event in the
evolution of insect mitochondrial genomes.
相似文献
3.
MF Perutz 《Current opinion in structural biology》1996,6(6):848-858
Several dominantly inherited, late onset, neurodegenerative diseases are due to expansion of CAG repeats, leading to expansion of glutamine repeats in the affected proteins. These proteins are of very different sizes and, with one exception, show no sequence homology to known proteins or to each other; their functions are unknown. In some, the glutamine repeat starts near the N-terminus, in another near the middle and in another near the C-terminus, but regardless of these differences, no disease has been observed in individuals with fewer than 37 repeats, and absence of disease has never been found in those with more than 41 repeats. Protein constructs with more than 41 repeats are toxic to E. coli and to CHO cells in culture, and they elicit ataxia in transgenic mice. These observations argue in favour of a distinct change of structure associated with elongation beyond 37–41 glutamine repeats. The review describes experiments designed to find out what these structures might be and how they could influence the properties of the proteins of which they form part. Poly-
-glutamines form pleated sheets of β-strands held together by hydrogen bonds between their amides. Incorporation of glutamine repeats into a small protein of known structure made it associate irreversibly into oligomers. That association took place during the folding of the protein molecules and led to their becoming firmly interlocked by either strand- or domain-swapping. Thermodynamic considerations suggest that elongation of glutamine repeats beyond a certain length may lead to a phase change from random coils to hydrogen-bonded hairpins. Possible mechanisms of expansion of CAG repeats are discussed in the light of looped DNA model structures. 相似文献
4.
5.
Using a battery of seven lectin-ferritin conjugates as probes for cell surface glycoconjugates, we have studied the pattern of plasmalemmal differentiation of cells in the embryonic rat pancreas from day 15 in utero to the early postpartum stage. Our results indicate that differentiation of plasmalemmal glycoconjugates on acinar, endocrine, and centroacinar cells is temporally correlated with development and is unique for each cell type, as indicated by lectin-ferritin binding. Specifically, (a) expression of adult cell surface saccharide phenotype can be detected on presumptive acinar cells as early as 15 d in utero, as indicated by soybean agglutinin binding, and precedes development of intracellular organelles characteristic of mature acinar cells; (b) maturation of the plasmalemma of acinar cells is reached after intracellular cytodifferentiation is completed, as indicated by appearance of Con A and fucoselectin binding sites only at day 19 of development; conversely, maturation of the endocrine cell plasmalemma is accompanied by "loss" (masking) of ricinus communis II agglutinin receptors; and (c) binding sites for fucose lectins and for soybean agglutinin are absent on endocrine and centroacinar cells at all stages examined. We conclude that acinar, centroacinar, and endocrine cells develop from a common progenitor cell(s) whose plasmalemmal carbohydrate composition resembles most closely that of the adult centroacinar cell. Finally, appearance of acinar lumina beginning at approximately 17 d in utero is accompanied by differenetiation of apical and basolateral plasmalemmal domains of epithelial cells, as indicated by enhanced binding of several lectin-ferritin conjugates to the apical plasmalemmal, a pattern that persists from this stage through adult life. 相似文献
6.
Shun‐Fu Chang Heng Jung Chen Kam‐Fai Lee Tseng‐Hsi Lin Ting‐Ying Huang Chu‐Shan Choe Li‐Tsen Lin Cheng‐Nan Chen 《Cellular microbiology》2013,15(10):1722-1734
Porphyromonas gingivalis is a major pathogen in the initiation and progression of periodontal disease, which is recognized as a common complication of diabetes. ICAM‐1 expression by human gingival fibroblasts (HGFs) is crucial for regulating local inflammatory responses in inflamed periodontal tissues. However, the effect of P. gingivalis in a high‐glucose situation in regulating HGF function is not understood. The P. gingivalis strain CCUG25226 was used to study the mechanisms underlying the modulation of HGF ICAM‐1 expression by invasion of high‐glucose‐treated P. gingivalis (HGPg). A high‐glucose condition upregulated fimA mRNA expression in P. gingivalis and increased its invasion ability in HGFs. HGF invasion with HGPg induced increases in the expression of ICAM‐1. By using specific inhibitors and short hairpin RNA (shRNA), we have demonstrated that the activation of p38 MAPK and Akt pathways is critical for HGPg‐induced ICAM‐1 expression. Luciferase reporters and chromatin immunoprecipitation assays suggest that HGPg invasion increases NF‐κB‐ and Sp1‐DNA‐binding activities in HGFs. Inhibition of NF‐κB and Sp1 activations blocked the HGPg‐induced ICAM‐1 promoter activity and expression. The effect of HGPg on HGF signalling and ICAM‐1 expression is mediated by CXC chemokine receptor 4 (CXCR4). Our findings identify the molecular pathways underlying HGPg‐dependent ICAM‐1 expression in HGFs, providing insight into the effect of P. gingivalis invasion in HGFs. 相似文献
7.
Fred Tsen Ayesha Bhatia Kathryn O'Brien Chieh-Fang Cheng Mei Chen Nissim Hay Bangyan Stiles David T. Woodley Wei Li 《Molecular and cellular biology》2013,33(24):4947-4959
Normal cells secrete heat shock protein 90 alpha (Hsp90α) in response to tissue injury. Tumor cells have managed to constitutively secrete Hsp90α during invasion and metastasis. The sole function of extracellular Hsp90α (eHsp90α) is to promote cell motility, a critical event for both wound healing and tumor progression. The mechanism of promotility action by eHsp90α, however, has remained elusive. A key issue is whether eHsp90α still acts as a chaperone outside the cells or is a new and bona fide signaling molecule. Here, we have provided evidence that eHsp90α utilizes a unique transmembrane signaling mechanism to promote cell motility and wound healing. First, subdomain II in the extracellular part of low-density lipoprotein receptor-related protein 1 (LRP-1) receives the eHsp90α signal. Then, the NPVY but not the NPTY motif in the cytoplasmic tail of LRP-1 connects eHsp90α signaling to serine 473 but not threonine 308 phosphorylation in Akt kinases. Individual knockdown of Akt1, Akt2, or Akt3 revealed the importance of Akt1 and Akt2 in eHsp90α-induced cell motility. Akt gene rescue experiments suggest that Akt1 and Akt2 work in concert, rather than independently, to mediate eHsp90α promotility signaling. Finally, Akt1 and Akt2 knockout mice showed impaired wound healing that cannot be corrected by topical application with the eHsp90α protein. 相似文献
8.
Wei‐Chun Cheng Yi‐Huey Chen Hon‐Tsen Yu J. Dale Roberts Yeong‐Choy Kam 《Ethology : formerly Zeitschrift fur Tierpsychologie》2013,119(4):286-295
Sequential polygyny is a reproductive strategy that allows males to continue to mate and compensates for the loss of future breeding opportunities incurred by parental care (i.e. egg attendance). Using the frog Kurixalus eiffengeri, we tested predictions that (1) attending males fathered two, overlapping clutches; and (2) that double clutching leads to improved offspring numbers. Using five microsatellite DNA markers, we genotyped 15 pairs of overlapping clutches, which differed slightly in developmental stage at a single egg‐laying site. Parentage analyses showed at least 12 of 15 pairs of overlapping egg clutches were sired by the attending male mated with different females, providing the first genetic evidence to support an earlier prediction that attending males sired both egg clutches. Field surveys found a low incidence of overlapping clutches (4.9% of 263 egg‐occupied stumps), suggesting sequential polygyny is uncommon. Stumps with multiple clutches contained significantly more eggs than stumps with single clutches but hatched similar number of tadpoles. Results suggest that continuous calling that attracts females during egg attendance is a reproductive tactic that maximizes mating opportunities. However, adoption of the sequential polygyny tactic may only result in marginal fitness gains for males that are traded off against average higher egg mortality in larger egg clutches. 相似文献
9.
Deng C Radu C Diab A Tsen MF Hussain R Cowdery JS Racke MK Thomas JA 《Journal of immunology (Baltimore, Md. : 1950)》2003,170(6):2833-2842
Infections often precede the development of autoimmunity. Correlation between infection with a specific pathogen and a particular autoimmune disease ranges from moderately strong to quite weak. This lack of correspondence suggests that autoimmunity may result from microbial activation of a generic, as opposed to pathogen-specific host-defense response. The Toll-like receptors, essential to host recognition of microbial invasion, signal through a common, highly conserved pathway, activate innate immunity, and control adaptive immune responses. To determine the influence of Toll/IL-1 signaling on the development of autoimmunity, the responses of wild-type (WT) mice and IL-1R-associated kinase 1 (IRAK1)-deficient mice to induction of experimental autoimmune encephalomyelitis were compared. C57BL/6 and B6.IRAK1-deficient mice were immunized with MOG 35-55/CFA or MOG 35-55/CpG DNA/IFA. WT animals developed severe disease, whereas IRAK1-deficient mice were resistant to experimental autoimmune encephalomyelitis, exhibiting little or no CNS inflammation. IRAK1-deficient T cells also displayed impaired Th1 development, particularly during disease induction, despite normal TCR signaling. These results suggest that IRAK1 and the Toll/IL-1 pathway play an essential role in T cell priming, and demonstrate one means through which innate immunity can control subsequent development of autoimmunity. These findings may also help explain the association between antecedent infection and the development or exacerbations of some autoimmune diseases. 相似文献
10.
Swantek JL Tsen MF Cobb MH Thomas JA 《Journal of immunology (Baltimore, Md. : 1950)》2000,164(8):4301-4306
Endotoxin triggers many of the inflammatory, hemodynamic, and hematological derangements of Gram-negative septic shock. Recent genetic studies in mice have identified the Toll-like receptor 4 as the transmembrane endotoxin signal transducer. The IL-1 intracellular signaling pathway has been implicated in Toll-like receptor signal transduction. LPS-induced activation of the IL-1 receptor-associated kinase (IRAK), and the influence of IRAK on intracellular signaling and cellular responses to endotoxin has not been explored in relevant innate immune cells. We demonstrate that LPS activates IRAK in murine macrophages. IRAK-deficient macrophages, in contrast, are resistant to LPS. Deletion of IRAK disrupts several endotoxin-triggered signaling cascades. Furthermore, macrophages lacking IRAK exhibit impaired LPS-stimulated TNF-alpha production, and IRAK-deficient mice withstand the lethal effects of LPS. These findings, coupled with the critical role for IRAK in IL-1 and IL-18 signal transduction, demonstrate the importance of this kinase and the IL-1/Toll signaling cassette in sensing and responding to Gram-negative infection. 相似文献