排序方式: 共有194条查询结果,搜索用时 15 毫秒
1.
2.
H. Seenu Srinatha Subbaraman Sriram Akshay K. Chakravarthy 《Biocontrol Science and Technology》2015,25(7):789-802
Four bacterial and one yeast species, cultured and identified as Stenotrophomonas maltophilia, Acinetobacter sp., Pseudomonas sp. and Ochrobactrum sp. and the yeast as Metschnikowia reukaufii, were isolated from the internal organs of four collections of field-sourced egg parasitoid, Trichogramma chilonis, obtained as parasitised Helicoverpa armigera eggs. Bacteria were identified through 16 rRNA amplification and sequencing. The single species of yeast was identified through internal transcribed spacer sequences. A single bacterial species could be isolated from each of the four T. chilonis collections; however, all four T. chilonis collections yielded the yeast, M. reukaufii. In order to study the influence of the association of each of the bacterial species and the yeast, microbe-free laboratory-bred populations of T. chilonis were fed with the individual cultures and fitness parameters as parasitisation vigour and female bias were studied in T. chilonis over 10 generations. T. chilonis fed with either S. maltophilia or Acinetobacter sp. and Pseudomonas sp. showed a mean percent increase in female ratio of 26.2%, 30% and 30.3% and mean percent parasitisation of H. armigera eggs significantly increased by 38%, 32.2% and 31.3%, respectively. However, T. chilonis fed with Acinetobacter sp. did not positively influence the two T. chilonis fitness factors. The ubiquitous yeast, M. reukaufii, which could be isolated from all four collections of T. chilonis, could significantly increase both female count and percent parasitism ratio by 22% and 65%, respectively. This study has opened the possibility of modulating the parasitisation fitness of laboratory-bred T. chilonis, prior to field release, using microbes associated with them in the wild. 相似文献
3.
Tammy Y. Carter Swetha Gadwala Ashish B. Chougule Anh P. N. Bui Alex C. Sanders Raghothama Chaerkady Nathaly Cormier Robert N. Cole Jeffrey H. Thomas 《Genesis (New York, N.Y. : 2000)》2019,57(6)
Src64 is required for actomyosin contraction during cellularization of the Drosophila embryonic blastoderm. The mechanism of actomyosin ring constriction is poorly understood even though a number of cytoskeletal regulators have been implicated in the assembly, organization, and contraction of these microfilament rings. How these cytoskeletal processes are regulated during development is even less well understood. To investigate the role of Src64 as an upstream regulator of actomyosin contraction, we conducted a proteomics screen to identify proteins whose expression levels are controlled by src64. Global levels of actin are reduced in src64 mutant embryos. Furthermore, we show that reduction of the actin isoform Actin 5C causes defects in actomyosin contraction during cellularization similar to those caused by src64 mutation, indicating that a relatively high level of Actin 5C is required for normal actomyosin contraction and furrow canal structure. However, reduction of Actin 5C levels only slows down actomyosin ring constriction rather than preventing it, suggesting that src64 acts not only to modulate actin levels, but also to regulate the actomyosin cytoskeleton by other means. 相似文献
4.
Kindlin Is Mechanosensitive: Force-Induced Conformational Switch Mediates Cross-Talk among Integrins
Zeinab Jahed Zainab Haydari Akshay Rathish Mohammad R.K. Mofrad 《Biophysical journal》2019,116(6):1011-1024
Mechanical stresses directly regulate the function of several proteins of the integrin-mediated focal adhesion complex as they experience intra- and extracellular forces. Kindlin is a largely overlooked member of the focal adhesion complex whose roles in cellular mechanotransduction are only recently being identified. Recent crystallographic experiments have revealed that kindlins can form dimers that bind simultaneously to two integrins, providing a mechanistic explanation of how kindlins may promote integrin activation and clustering. In this study, using the newly identified molecular structure, we modeled the response of the kindlin2 dimer in complex with integrin β1 to mechanical cytoskeletal forces on integrins. Using molecular dynamics simulations, we show that forces on integrins are directly transmitted to the kindlin2 dimerization site, resulting in a shift in an R577-S550/E553 interaction network at this site. Under force, R577 on one protomer switches from interacting with S550 to forming new hydrogen bonds with E553 on the neighboring protomer, resulting in the strengthening of the kindlin2 dimer in complex with integrin β1. This force-induced strengthening is similar to the catch-bond mechanisms that have previously been observed in other adhesion molecules. Based on our results, we propose that the kindlin2 dimer is mechanosensitive and can strengthen integrin-mediated focal adhesions under force by shifting the interactions at its dimerization sites. 相似文献
5.
Generation of a tamoxifen inducible Tnnt2MerCreMer knock‐in mouse model for cardiac studies 下载免费PDF全文
Jianyun Yan Nishat Sultana Lu Zhang David S. Park Akshay Shekhar Jun Hu Lei Bu Chen‐Leng Cai 《Genesis (New York, N.Y. : 2000)》2015,53(6):377-386
Tnnt2, encoding thin‐filament sarcomeric protein cardiac troponin T, plays critical roles in heart development and function in mammals. To develop an inducible genetic deletion strategy in myocardial cells, we generated a new Tnnt2:MerCreMer (Tnnt2MerCreMer/+) knock‐in mouse. Rosa26 reporter lines were used to examine the specificity and efficiency of the inducible Cre recombinase. We found that Cre was specifically and robustly expressed in the cardiomyocytes at embryonic and adult stages following tamoxifen induction. The knock‐in allele on Tnnt2 locus does not impact cardiac function. These results suggest that this new Tnnt2MerCreMer/+ mouse could be applied towards the temporal genetic deletion of genes of interests in cardiomyocytes with Cre‐LoxP technology. The Tnnt2MerCreMer/+ mouse model also provides a useful tool to trace myocardial lineage during development and repair after cardiac injury. genesis 53:377–386, 2015. © 2015 Wiley Periodicals, Inc. 相似文献
6.
Jacqueline Y. Quinn Robert Sidney Cox III Aaron Adler Jacob Beal Swapnil Bhatia Yizhi Cai Joanna Chen Kevin Clancy Michal Galdzicki Nathan J. Hillson Nicolas Le Novère Akshay J. Maheshwari James Alastair McLaughlin Chris J. Myers Umesh P Matthew Pocock Cesar Rodriguez Larisa Soldatova Guy-Bart V. Stan Neil Swainston Anil Wipat Herbert M. Sauro 《PLoS biology》2015,13(12)
Synthetic Biology Open Language (SBOL) Visual is a graphical standard for genetic engineering. It consists of symbols representing DNA subsequences, including regulatory elements and DNA assembly features. These symbols can be used to draw illustrations for communication and instruction, and as image assets for computer-aided design. SBOL Visual is a community standard, freely available for personal, academic, and commercial use (Creative Commons CC0 license). We provide prototypical symbol images that have been used in scientific publications and software tools. We encourage users to use and modify them freely, and to join the SBOL Visual community: http://www.sbolstandard.org/visual. 相似文献
7.
Simon Gemble Akshay Ahuja Géraldine Buhagiar-Labarchède Rosine Onclercq-Delic Julien Dairou Denis S. F. Biard Sarah Lambert Massimo Lopes Mounira Amor-Guéret 《PLoS genetics》2015,11(7)
Genome stability is jeopardized by imbalances of the dNTP pool; such imbalances affect the rate of fork progression. For example, cytidine deaminase (CDA) deficiency leads to an excess of dCTP, slowing the replication fork. We describe here a novel mechanism by which pyrimidine pool disequilibrium compromises the completion of replication and chromosome segregation: the intracellular accumulation of dCTP inhibits PARP-1 activity. CDA deficiency results in incomplete DNA replication when cells enter mitosis, leading to the formation of ultrafine anaphase bridges between sister-chromatids at “difficult-to-replicate” sites such as centromeres and fragile sites. Using molecular combing, electron microscopy and a sensitive assay involving cell imaging to quantify steady-state PAR levels, we found that DNA replication was unsuccessful due to the partial inhibition of basal PARP-1 activity, rather than slower fork speed. The stimulation of PARP-1 activity in CDA-deficient cells restores replication and, thus, chromosome segregation. Moreover, increasing intracellular dCTP levels generates under-replication-induced sister-chromatid bridges as efficiently as PARP-1 knockdown. These results have direct implications for Bloom syndrome (BS), a rare genetic disease combining susceptibility to cancer and genomic instability. BS results from mutation of the BLM gene, encoding BLM, a RecQ 3’-5’ DNA helicase, a deficiency of which leads to CDA downregulation. BS cells thus have a CDA defect, resulting in a high frequency of ultrafine anaphase bridges due entirely to dCTP-dependent PARP-1 inhibition and independent of BLM status. Our study describes previously unknown pathological consequences of the distortion of dNTP pools and reveals an unexpected role for PARP-1 in preventing DNA under-replication and chromosome segregation defects. 相似文献
8.
Yann C. Klimentidis Akshay Chougule Amit Arora Alexis C. Frazier-Wood Chiu-Hsieh Hsu 《PLoS genetics》2015,11(5)
Elevated plasma triglyceride (TG) levels are an established risk factor for type-2 diabetes (T2D). However, recent studies have hinted at the possibility that genetic risk for TG may paradoxically protect against T2D. In this study, we examined the association of genetic risk for TG with incident T2D, and the interaction of baseline TG with TG genetic risk on incident T2D in 13,247 European-Americans (EA) and 3,238 African-Americans (AA) from three prospective cohort studies. A TG genetic risk score (GRS) was calculated based on 31 validated single nucleotide polymorphisms (SNPs). We considered several baseline covariates, including body- mass index (BMI) and lipid traits. Among EA and AA, we find, as expected, that baseline levels of TG are strongly positively associated with incident T2D (p<2 x 10-10). However, the TG GRS is negatively associated with T2D (p=0.013), upon adjusting for only race, in the full dataset. Upon additionally adjusting for age, sex, BMI, high-density lipoprotein cholesterol and TG, the TG GRS is significantly and negatively associated with T2D incidence (p=7.0 x 10-8), with similar trends among both EA and AA. No single SNP appears to be driving this association. We also find a significant statistical interaction of the TG GRS with TG (pinteraction=3.3 x 10-4), whereby the association of TG with incident T2D is strongest among those with low genetic risk for TG. Further research is needed to understand the likely pleiotropic mechanisms underlying these findings, and to clarify the causal relationship between T2D and TG. 相似文献
9.
10.