Two-step binding of eukaryotic ribosomes to brome mosaic virus RNA3

Although brome mosaic virus RNA3 has only one translatable cistron, it can bind two 80S ribosomes at initiation. One ribosome binds at the first AUG codon (base 92-94). The other binds nearer the 5' end at an entry or holding site. Disome formation is thus unrelated to a silent cistron approximately 1,000 bases downstream.     

Inhibition of mRNA binding to ribosomes by localized activation of dsRNA-dependent protein kinase

The initiation of protein synthesis can be regulated in mammalian cells by protein kinases which phosphorylate the alpha subunit of initiation factor eIF-2. This phosphorylation results in a block in the recycling of eIF-2 and in the inhibition of messenger RNA binding to 80S initiation complexes. After eIF-2 alpha is phosphorylated, the mRNA becomes associated with 48S complexes consisting of a 40S ribosomal subunit, eIF-2 (alpha P), GDP and Met-tRNAf. One of the eIF-2 alpha kinases is activated by low concentrations of double-stranded RNA (dsRNA). This kinase (PKds) is present at a basal level in all mammalian cells investigated and its synthesis is induced in cells treated with interferon. The PKds may be involved in the inhibition of translation of viral mRNA in interferon-treated cells infected with RNA viruses, as it is activated by viral replicative complexes. It is not known, however, if the activated PKds preferentially inhibits the translation of viral mRNA when cellular protein synthesis proceeds at a normal rate in infected cells. We now report that mRNA covalently linked to dsRNA is preferentially inhibited from binding to 80S complexes by a localized activation of PKds. This suggests that in interferon-treated cells the binding of some nascent viral mRNAs to functional initiation complexes may be preferentially inhibited by a similar mechanism.     

Malignant transformation by a eukaryotic initiation factor subunit that binds to mRNA 5' cap

Eukaryotic cellular mRNAs have a 5' cap structure (m7 GpppX) that facilitates binding to ribosomes and is required for efficient translation. A specific initiation factor, eIF-4F, mediates the function of the cap and consists of three subunits, one of which, eIF-4E, binds the cap. This subunit is present in limiting amounts in the cell, and is thought to be regulated by phosphorylation: decreased phosphorylation of eIF-4E following various treatments correlates with a decrease in cellular translation rate. These observations suggest that eIF-4E lies on the mitogenic signal transduction pathway, and we reasoned that overexpression of eIF-4E might profoundly affect cellular growth properties. We report here that overexpression of eIF-4E in NIH 3T3 and Rat 2 fibroblasts causes their tumorigenic transformation as determined by three criteria: formation of transformed foci on a monolayer of cells; anchorage-independent growth; and tumour formation in nude mice.     

Pathogenic bacteria attach to human fibronectin through a tandem beta-zipper

Staphylococcus aureus and Streptococcus pyogenes, two important human pathogens, target host fibronectin (Fn) in their adhesion to and invasion of host cells. Fibronectin-binding proteins (FnBPs), anchored in the bacterial cell wall, have multiple Fn-binding repeats in an unfolded region of the protein. The bacterium-binding site in the amino-terminal domain (1-5F1) of Fn contains five sequential Fn type 1 (F1) modules. Here we show the structure of a streptococcal (S. dysgalactiae) FnBP peptide (B3) in complex with the module pair 1F12F1. This identifies 1F1- and 2F1-binding motifs in B3 that form additional antiparallel beta-strands on sequential F1 modules-the first example of a tandem beta-zipper. Sequence analyses of larger regions of FnBPs from S. pyogenes and S. aureus reveal a repeating pattern of F1-binding motifs that match the pattern of F1 modules in 1-5F1 of Fn. In the process of Fn-mediated invasion of host cells, therefore, the bacterial proteins seem to exploit the modular structure of Fn by forming extended tandem beta-zippers. This work is a vital step forward in explaining the full mechanism of the integrin-dependent FnBP-mediated invasion of host cells.     

5'-Terminal 7-methylguanosine in eukaryotic mRNA is required for translation.

Unmethylated reovirus and VSV mRNAs are specifically methylated to form 5'-terminal structures of the type, m-7-G(5')ppp(5')N by protein synthesising extracts prepared from wheat germ and mouse L cells. Reticulocyte mRNA also contains 5'-terminal m-7-G. MRNAs having 5'-terminal m-7-G stimulate protein synthesis in vitro. Removal of m-7-G by beta-elimination abolishes translation of the mRNAs.     

圆形槽波导到圆波导结的分析

用有限元法分析了圆形槽波导到圆波导结这一复杂结构的电磁特性．为了避免伪模式的产生,有限元法的基函数采用的是矢量基函数．利用完全匹配层(PML)来解决槽波导无限域结构的截断问题．有限元有限元法法的分析得出了这一波导结中圆形槽波导端口TE11^=0=模和圆波导端口TE11^0模之间的模式散射参数(5参数)随离散频率点和耦合结构尺寸变化的结果,分析结果为圆形槽波导谐振腔或振荡器的设计提供了依据．     

Internal initiation of translation of eukaryotic mRNA directed by a sequence derived from poliovirus RNA

Poliovirus RNA is naturally uncapped, therefore its translation must proceed via a cap-independent mechanism. Translation initiation on poliovirus RNA occurs by binding of ribosomes to an internal sequence within the 5' noncoding region. This novel mechanism of initiation may explain the disparate translation of several other eukaryotic messenger RNAs.     

深化教学改革,重视实验课程建设

实验课的课程建设是实验教学改革的关键,文章阐述了实验课程建设在教学改革中的地位和作用,并就如何搞好实验课程建设和教育创新,谈了自己的看法.     

Inability of Rous sarcoma virus to cause sarcomas in the avian embryo

The injection of Rous sarcoma virus (RSV) into the wing web of newly hatched chicks causes a rapidly growing sarcomatous tumour which is palpable within 1 week of inoculation; and cultures of fibroblasts derived from chick embryos (CEF) and infected with RSV become rapidly transformed. Genetic studies have determined that expression of a single viral gene, designated v-src, is necessary for neoplastic transformation. This gene codes for a 60,000-molecular weight phosphoprotein termed pp60SPC , which possesses a protein kinase activity that phosphorylates polypeptides on tyrosine residues and is constitutively expressed in infected CEF cells. It has been suggested that transformation, and possibly tumorigenesis, may result solely from the consequences of this increase in tyrosine phosphorylations. The pathogenicity of RSV in chick embryos in ovo is less clear. Murphy and Rous suggested that RSV may have caused tumours in "various tissues" of "some embryos", but the subsequent studies of Milford and Duran - Reynals , as well as several other laboratories, failed to find any evidence of intraembryonic tumours in RSV-infected early embryos. The findings of Duran - Reynals , if correct, cannot be explained easily in view of our present understanding of RSV tumorigenicity. Thus, we have re-examined the interaction of RSV with the avian embryo and confirm here that RSV is nontumorigenic and non-teratogenic when microinjected into day 4 chicken embryos. In addition, we found that (1) the virus not only replicates in the embryo, but it also expresses an active src-specific protein kinase and (2) once the cells from the infected limbs are disrupted and placed in culture, they are capable of expressing the transformed phenotype after a 24-h delay.