Virological survey of rhesus monkeys in China

A virological survey of rhesus monkeys captured in China for 13 viruses and/or antibodies was performed. Antigens used were SFV, SF40, HSV-1, Sa11, measles, vaccinia, epidemic or simian hemorrhagic fever, Langat, Kunming, poliomyelitis, HIV, SV41 and rubella. Monkeys were from Sichuan, Hunan, Guizhou, Yunnan and Guangxi provinces. Antibody was detected to all the listed viruses except HIV, SV41 and rubella. Both SFV and SV40 were recovered from monkeys, but H. simiae, LCM and coxsackieviruses were not.     

Mutation mechanism of chlorophyll-less barley mutant <Emphasis Type="Italic">NYB</Emphasis>

NYB is chlorophyll-less barley mutant, which is controlled by a recessive nuclear gene. The mutation mechanism is revealed. The activities of enzymes transforming 5-aminolevulinic acid into protochlorophyllide were the same in both NYB and the wild type (WT), but the activity of the protochlorophyllide oxidoreductase (POR) in WT was much higher than that of NYB. Most of the photosystem 2 apoproteins were present in both WT and NYB, suggesting that the capability of protein synthesis was probably fully preserved in the mutant. Thus chlorophyll (Chl) biosynthesis in NYB was hampered at conversion form protochlorophyllide (Pchlide) into chlorophyllide. The open reading frame of porB gene in NYB was inserted with a 95 bp fragment, which included a stop codon. The NYB mutant is a very useful material for studies of Chl biosynthesis, chloroplast signalling, and structure of light-harvesting POR-Pchlide complex (LHPP).     

Photoperiodic reaction in the beet webworm Loxostege sticticalis L. (Pyraloidea, Crambidae) from eastern and western parts of its Eurasian range

The beet webworm, Loxostege sticticalis L., is a very dangerous polyphagous insect pest whose outbreaks periodically occur in southern Russia and northern China. The aim of our work was to describe the photoperiodic response of beet webworm populations from western (Krasnodar Territory and Rostov Province) and eastern [Buryatia and China (Hebei Province)] parts of the pest range. The insects were reared under constant photoperiods of 12–18 h and constant temperatures of 19–25°C. Incidence of diapause at different photoperiods did not show any considerable geographic differences, and the critical day length at which 50% of prepupae arrested their development was about 14–15 h in all the populations studied at experimental temperatures. The results obtained agree with the hypothesis on the existence of an area (or areas) where the pest survives during adverse periods and wherefrom it spreads when an outbreak begins (Saulich et al., 1983; Goryshin et al., 1986). Presumably, the larger part of the pest native habitats (to the north of the steppe zone) is occupied by temporary populations, incapable of surviving for long periods without an inflow of migrants from more southerly steppe regions.     

Roles of OsCKI1, a rice casein kinase I, in root development and plant hormone sensitivity

Casein kinases are critical in cell division and differentiation across species. A rice cDNA fragment encoding a putative casein kinase I (CKI) was identified via cDNA macroarray under brassinosteroid (BR) treatment, and a 1939-bp full-length cDNA, OsCKI1, was isolated and found to encode a putative 463-aa protein. RT-PCR and Northern blot analysis indicated that OsCKI1 was constitutively expressed in various rice tissues and upregulated by treatments with BR and abscisic acid (ABA). Enzymatic assay of recombinant OsCKI1 proteins expressed in Escherichia coli showed that the protein was capable of phosphorylating casein. The physiological roles of OsCKI1 were studied through antisense transgenic approaches, and homozygous transgenic plants showed abnormal root development, including fewer lateral and adventitious roots, and shortened primary roots as a result of reduced cell elongation. Treatment of wild-type plants with CKI-7, a specific inhibitor of CKI, also confirmed these functions of OsCKI1. Interestingly, in transgenic and CKI-7-treated plants, exogenously supplied IAA could restore normal root development, and measurement of free IAA content in CKI-deficient primary and adventitious roots revealed altered auxin content, indicating that OsCKI1 is involved in auxin metabolism or that it may affect auxin levels. Transgenic plants were less sensitive than control plants to ABA or BR treatment during germination, suggesting that OsCKI1 may be involved in various hormone-signaling pathways. OsCKI1-GFP fusion studies revealed the localization of OsCKI1 to the nucleus, suggesting a possible involvement in regulation of gene expression. In OsCKI1-deficient plants, differential gene expression was investigated using cDNA chip technology, and results indicated that genes related to signal transduction and hormone metabolism were indeed with altered expression.     

Blockade of L-type voltage-gated Ca channel inhibits ischemia-induced neurogenesis by down-regulating iNOS expression in adult mouse

Neurogenesis in the adult mammalian hippocampus may contribute to repairing the brain after injury. The signals that regulate neurogenesis in the dentate gyrus following ischemic stroke insult are not well known. We have previously reported that inducible nitric oxide synthase (iNOS) expression is necessary for ischemia-stimulated neurogenesis in the adult dentate gyrus. Here, we show that mice subjected to 90 min of middle cerebral artery occlusion (MCAO) significantly increased the number of new neurons and up-regulated iNOS expression in the dentate gyrus. Blockade of the L-type voltage-gated Ca(2+) channel (L-VGCC) prevented neurogenesis in the dentate gyrus and subventricular zone (SVZ), and down-regulated iNOS expression in the dentate gyrus after cerebral ischemia. This study suggests that Ca(2+) influx through L-VGCC is involved in ischemia-induced neurogenesis by up-regulating iNOS expression.     

D2 Dopamine Receptors Stimulate Mitogenesis Through Pertussis Toxin-Sensitive G Proteins and Ras-Involved ERK and SAP/JNK Pathways in Rat C6-D2L Glioma Cells

Abstract: Dopamine D2 receptors are members of the G protein-coupled receptor superfamily and are expressed on both neurons and astrocytes. Using rat C6 glioma cells stably expressing the rat D2L receptor, we show here that dopamine (DA) can activate both the extracellular signal-regulated kinase (ERK) and c-Jun NH₂-terminal kinase (JNK) pathways through a mechanism involving D2 receptor-G protein complexes and the Ras GTP-binding protein. Agonist binding to D2 receptors rapidly activated both kinases within 5 min, reached a maximum between 10 and 15 min, and then gradually decreased by 60 min. Maximal activation of both kinases occurred with 100 nM DA, which produced a ninefold enhancement of ERK activity and a threefold enhancement of JNK activity. DA-induced kinase activation was prevented by either (+)-butaclamol, a selective D2 receptor antagonist, or pertussis toxin, an uncoupler of G proteins from receptors, but not by (?)-butaclamol, the inactive isomer of (+)-butaclamol. Cotransfection of RasN17, a dominant negative Ras mutant, prevented DA-induced activation of both ERK and JNK. PD098059, a specific MEK1 inhibitor, also blocked ERK activation by DA. Transfection of SEK1(K → R) vector, a dominant negative SEK1 mutant, specifically prevented DA-induced JNK activation and subsequent c-Jun phosphorylation without effect on ERK activation. Furthermore, stimulation of D2 receptors promoted [³H]thymidine incorporation with a pattern similar to that for kinase activation. DA mitogenesis was tightly linked to Ras-dependent mitogen-activated protein kinase (MAPK) and JNK pathways. Transfection with RasN17 and application of PD098059 blocked DA-induced DNA synthesis. Transfection with FlagΔ169, a dominant negative c-Jun mutant, also prevented stimulation of [³H]thymidine incorporation by DA. The demonstration of D2 receptor-stimulated MAPK pathways may help to understand dopaminergic physiological functions in the CNS.