蜜蜂人工代用花粉中适宜钙磷水平的初步研究

钙磷是蜜蜂饲粮中必需的常量元素。为了探讨蜜蜂人工代用花粉中适宜的钙磷水平,本试验选取蜂王、群势基本一致的意大利蜜蜂Apis mellifera ligustica Spinola 70群,随机分为14个组,每组5群蜂,前12组饲喂采用均匀设计法配制的不同钙磷水平的人工代用花粉。第13组饲喂不加钙磷的人工代用花粉为负对照,第14组饲喂纯油菜花粉为正对照。试验从春繁开始,到刺槐流蜜期结束为止。试验期间测定蜂群的采食量、蜂群群势、幼蜂初生重,成蜂蜂体组织内钙磷含量。结果表明:当人工代用花粉中钙磷水平分别为0,0.65%时,蜂群的采食量、蜂群群势、幼蜂初生重均取得最大值;成蜂蜂体组织内钙含量与人工代用花粉中钙磷含量成正相关,成蜂蜂体组织内磷含量与人工代用花粉中钙磷含量之间没有相关性。     

不同光质对烟草叶片组织结构及Rubisco羧化酶活性和rbc、rca基因表达的影响

通过对烟草植株覆盖白、红、黄、蓝、紫色滤膜获得不同光质,研究了烟草叶片在7～70d的生长发育期内,不同光质处理对烟叶组织结构特征、核酮糖1,5-二磷酸羧化酶/加氧酶（Rubisco）羧化酶活性、Rubisco基因（rbc）表达及其活化酶（Rca）基因（rca）表达的影响。结果表明,与黄膜处理下生长的烟叶相比,红、蓝、紫膜处理下生长的烟叶有较高的叶片厚度、栅栏组织厚度、海绵组织厚度、栅栏细胞密度和较小的组织空隙率。此外,红、蓝、紫膜处理的叶片有较高的Rubis-co羧化酶活性和净光合速率及较强的rbc和rca基因表达。实验结果表明不同光质对烟草叶片的组织结构特征有显著影响,光质可能通过影响Rubisco羧化酶活性进而影响叶片光合效率,而光质、叶片组织结构和光合效率之间存在某种程度的相互联系。     

饲粮蛋白质水平对蜂群繁殖性能的影响

本试验旨在研究饲料蛋白质水平对蜜蜂产浆期繁殖性能的影响。选择35群群势、蜂王年龄和质量一致的意大利蜜蜂Apis mellifera L.,随机分为7组,分别饲喂蛋白质水平为15%、20%、25%、30%、35%及40%的试验饲粮并以油菜花粉作为对照,测定各组蜂群的繁殖性能。结果表明,试验前期,饲粮蛋白质水平对蜂群群势有显著性影响,然而在试验中后期,则无显著影响(P>0.05);随着饲粮蛋白质水平的增加,蜂王产卵力和工蜂初生重呈先升高后降低的变化趋势,与对照组相比差异不显著(P>0.05)。     

Orderly order in protein intrinsic disorder distribution: disorder in 3500 proteomes from viruses and the three domains of life

Intrinsically disordered proteins and intrinsically disordered protein regions are highly abundant in nature. However, the quantitative and qualitative measures of protein intrinsic disorder in species with known genomes are still not available. Furthermore, although the correlation between high fraction of disordered residues and advanced species has been reported, the details of this correlation and the connection between the disorder content and proteome complexity have not been reported as of yet. To fill this gap, we analysed entire proteomes of 3484 species from three domains of life (archaea, bacteria and eukaryotes) and from viruses. Our analysis revealed that the evolution process is characterized by distinctive patterns of changes in the protein intrinsic disorder content. We are showing here that viruses are characterized by the widest spread of the proteome disorder content (the percentage of disordered residues ranges from 7.3% in human coronavirus NL63 to 77.3% in Avian carcinoma virus). For several organisms, a clear correlation is seen between their disorder contents and habitats. In multicellular eukaryotes, there is a weak correlation between the complexity of an organism (evaluated as a number of different cell types) and its overall disorder content. For both the prokaryotes and eukaryotes, the disorder content is generally independent of the proteome size. However, disorder shows a sharp increase associated with the transition from prokaryotic to eukaryotic cells. This suggests that the increased disorder content in eukaryotic proteomes might be used by nature to deal with the increased cell complexity due to the appearance of the various cellular compartments.     

Rad51 presynaptic filament stabilization function of the mouse Swi5-Sfr1 heterodimeric complex

Homologous recombination (HR) represents a major error-free pathway to eliminate pre-carcinogenic chromosomal lesions. The DNA strand invasion reaction in HR is mediated by a helical filament of the Rad51 recombinase assembled on single-stranded DNA that is derived from the nucleolytic processing of the primary lesion. Recent studies have found that the human and mouse Swi5 and Sfr1 proteins form a complex that influences Rad51-mediated HR in cells. Here, we provide biophysical evidence that the mouse Swi5-Sfr1 complex has a 1:1 stoichiometry. Importantly, the Swi5-Sfr1 complex, but neither Swi5 nor Sfr1 alone, physically interacts with Rad51 and stimulates Rad51-mediated homologous DNA pairing. This stimulatory effect stems from the stabilization of the Rad51-ssDNA presynaptic filament. Moreover, we provide evidence that the RSfp (rodent Sfr1 proline rich) motif in Sfr1 serves as a negative regulatory element. These results thus reveal an evolutionarily conserved function in the Swi5-Sfr1 complex and furnish valuable information as to the regulatory role of the RSfp motif that is specific to the mammalian Sfr1 orthologs.     

Common chaperone activity in the G-domain of trGTPase protects L11�CL12 interaction on the ribosome

Translational GTPases (trGTPases) regulate all phases of protein synthesis. An early event in the interaction of a trGTPase with the ribosome is the contact of the G-domain with the C-terminal domain (CTD) of ribosomal protein L12 (L12-CTD) and subsequently interacts with the N-terminal domain of L11 (L11-NTD). However, the structural and functional relationships between L12-CTD and L11-NTD remain unclear. Here, we performed mutagenesis, biochemical and structural studies to identify the interactions between L11-NTD and L12-CTD. Mutagenesis of conserved residues in the interaction site revealed their role in the docking of trGTPases. During docking, loop62 of L11-NTD protrudes into a cleft in L12-CTD, leading to an open conformation of this domain and exposure of hydrophobic core. This unfavorable situation for L12-CTD stability is resolved by a chaperone-like activity of the contacting G-domain. Our results suggest that all trGTPases—regardless of their different specific functions—use a common mechanism for stabilizing the L11-NTD•L12-CTD interactions.     

High altitude adaptation in Daghestani populations from the Caucasus

We have surveyed 15 high-altitude adaptation candidate genes for signals of positive selection in North Caucasian highlanders using targeted re-sequencing. A total of 49 unrelated Daghestani from three ethnic groups (Avars, Kubachians, and Laks) living in ancient villages located at around 2,000 m above sea level were chosen as the study population. Caucasian (Adygei living at sea level, N = 20) and CEU (CEPH Utah residents with ancestry from northern and western Europe; N = 20) were used as controls. Candidate genes were compared with 20 putatively neutral control regions resequenced in the same individuals. The regions of interest were amplified by long-PCR, pooled according to individual, indexed by adding an eight-nucleotide tag, and sequenced using the Illumina GAII platform. 1,066 SNPs were called using false discovery and false negative thresholds of ~6%. The neutral regions provided an empirical null distribution to compare with the candidate genes for signals of selection. Two genes stood out. In Laks, a non-synonymous variant within HIF1A already known to be associated with improvement in oxygen metabolism was rediscovered, and in Kubachians a cluster of 13 SNPs located in a conserved intronic region within EGLN1 showing high population differentiation was found. These variants illustrate both the common pathways of adaptation to high altitude in different populations and features specific to the Daghestani populations, showing how even a mildly hypoxic environment can lead to genetic adaptation.     

Neuroprotective Effects of New Protein Kinase C Activator TPPB Against Aβ25–35 Induced Neurotoxicity in PC12 Cells

Alzheimer's disease (AD) is pathologically characterized by presence of senile plaques in the hippocampus, which are composed mainly of extracellular deposition of a polypeptide known as the beta amyloid, the Aβ. It has been demonstrated on numerous occasions that it was the deposition and aggregation of this Aβ peptide that cause neuronal dysfunction and even finally, the dementia. Lowering the deposition of Aβ or decreasing its neurotoxicity has long been one of the purposes of AD therapy. In previous study, we reported that protein kinase C (PKC) activator TPPB could regulate APP processing by increasing α-secretase activity. In this study we further investigated the potential neuroprotective effect of TPPB against Aβ(25-35)-induced neurotoxicity in PC12 cells. The results indicated that TPPB at concentration of 1?μM could antagonize Aβ(25-35) induced cell damage as evidenced by MTT assays, LDH release and by morphological changes. Furthermore, the neuroprotection in cell viability can be blocked by inhibitors of PKC, Akt and MAPK. The experiment also indicated that TPPB could increase the phosphorylation of Akt, PKC, MARCKS and MAPK, which were inhibited by Aβ(25-35) treatment. Finally, TPPB inhibited the activation of caspase-3 induced by Aβ(25-35). Taken together, the experiment here implies that TPPB has a role against Aβ(25-35)-induced neurotoxicity in PC12 cells and may suggest its therapeutic potential in AD.