The air-puff evoked escape behavior of the cricket, Gryllus bimaculatus, was investigated. Crickets almost always escaped away from the stimulus source. In an optimal condition, the mean escape direction was 162° opposite to the stimulus source. Stronger (higher velocity) air-puff elicited an escape in larger number of crickets. However, the escape direction became incorrect when the stimulus was too strong.Crickets with bilateral cercal ablation did not show any escape to an air-puff, while unilaterally ablated ones did respond to the same stimulus with an escape. However, the response rate of animals with unilateral cercal ablation was lower than that in intact animals. Although the mean escape direction of the crickets with unilateral cercal ablation was still opposite to the stimulus source, the direction was not so accurate as in intact animals.About 6 days after the unilateral cercal ablation, the response rate showed a statistically significant compensational recovery. On the other hand, 14 days were necessary for the recovery of the escape direction. Information which regulating the response rate and the behavioral orientation is likely being processed in different neural pathways.
The movement protein (MP) of Tomato mosaic virus (ToMV) was reported previously by us to be phosphorylated in vitro by a cellular protein kinase(s) that exhibited several characteristics of casein kinase 2 (CK2). To characterize further this CK2-like cellular kinase, we have cloned cDNAs encoding the CK2 catalytic subunit from tobacco and compared the properties of the recombinant protein with those of the CK2-like cellular kinase. The recombinant CK2 catalytic subunit formed a complex with ToMV MP and phosphorylated it, similar to the CK2-like cellular kinase. Phosphoamino acid analyses of various mutant MPs altered near the C terminus revealed that the recombinant CK2 catalytic subunit phosphorylated serine-261, while the CK2-like cellular kinase phosphorylated both serine-261 and threonine-256. Both kinases were suggested to phosphorylate an additional serine residue(s) in regions other than the C-terminal peptide. The results are consistent with our previous prediction of involvement of CK2 in phosphorylation of ToMV MP.
Our results demonstrate that the overexpression of SOCS-5 does not inhibit Th2 response, but rather augments the phenotype of the asthma model in vivo. This finding throws into question the therapeutic utility of using enhancement of SOCS-5 expression for Th2-dominant disease.
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