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首页> 外文期刊>Molecular and Cellular Biology >p38 Mitogen-Activated Protein Kinase Can Be Involved in Transforming Growth Factor β Superfamily Signal Transduction in Drosophila Wing Morphogenesis
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p38 Mitogen-Activated Protein Kinase Can Be Involved in Transforming Growth Factor β Superfamily Signal Transduction in Drosophila Wing Morphogenesis

机译：p38丝裂原激活的蛋白激酶可参与果蝇翼形态发生中的转化生长因子β超家族信号转导。

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p38 mitogen-activated protein kinase (p38) has been extensively studied as a stress-responsive kinase, but its role in development remains unknown. The fruit fly, Drosophila melanogaster, has two p38 genes, D-p38a and D-p38b. To elucidate the developmental function of the Drosophilap38’s, we used various genetic and pharmacological manipulations to interfere with their functions: expression of a dominant-negative form of D-p38b, expression of antisense D-p38b RNA, reduction of theD-p38 gene dosage, and treatment with the p38 inhibitor SB203580. Expression of a dominant-negative D-p38b in the wing imaginal disc caused a decapentaplegic (dpp)-like phenotype and enhanced the phenotype of a dpp mutant. Dpp is a secretory ligand belonging to the transforming growth factor β superfamily which triggers various morphogenetic processes through interaction with the receptor Thick veins (Tkv). Inhibition of D-p38b function also caused the suppression of the wing phenotype induced by constitutively active Tkv (TkvCA). Mosaic analysis revealed that D-p38b regulates the Tkv-dependent transcription of theoptomotor-blind (omb) gene in non-Dpp-producing cells, indicating that the site of D-p38b action is downstream of Tkv. Furthermore, forced expression of TkvCA induced an increase in the phosphorylated active form(s) of D-p38(s). These results demonstrate that p38, in addition to its role as a transducer of emergency stress signaling, may function to modulate Dpp signaling.
机译：p38促分裂原活化蛋白激酶（p38）作为应激反应激酶已得到广泛研究，但其在发育中的作用仍然未知。果蝇 Drosophila melanogaster 有两个p38基因， D-p38a 和 D-p38b 。为了阐明果蝇p38的发育功能，我们使用了多种遗传和药理学操作来干扰其功能：D-p38b的显性负型表达，反义D-p38b RNA的表达，减少 D-p38 基因的剂量，并用p38抑制剂SB203580治疗。机翼假体盘中显性阴性D-p38b的表达引起 decapentaplegic （ dpp ）样表型，并增强了 dpp 突变体。 Dpp是属于转化生长因子β超家族的分泌性配体，其通过与受体粗静脉（Tkv）的相互作用触发各种形态发生过程。 D-p38b功能的抑制还导致组成性活性Tkv（Tkv CA ）诱导的机翼表型受到抑制。镶嵌分析表明，D-p38b调节非Dpp产生细胞中光致盲（ omb ）基因的Tkv依赖性转录，表明D的位点-p38b动作在Tkv的下游。此外，Tkv CA 的强制表达诱导了D-p38磷酸化活性形式的增加。这些结果表明，p38除了其作为紧急压力信号转导子的作用外，还可以起到调节Dpp信号转导的作用。

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