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虾肝胰腺中 II 型卵黄生成抑制激素抑制卵黄蛋白原转录的机制:GC/cGMP 途径与不同 MAPK 依赖性级联反应的串扰。

Mechanisms for type-II vitellogenesis-inhibiting hormone suppression of vitellogenin transcription in shrimp hepatopancreas: Crosstalk of GC/cGMP pathway with different MAPK-dependent cascades.

机构信息

CAS Key Laboratory of Tropical Marine Bio-resources and Ecology (LMB); Guangdong Provincial Key Laboratory of Applied Marine Biology (LAMB), South China Sea Institute of Oceanology, Chinese Academy of Sciences, Guangzhou, China.

South China Sea Bio-Resource Exploitation and Utilization Collaborative Innovation Center, Guangzhou, China.

出版信息

PLoS One. 2018 Mar 28;13(3):e0194459. doi: 10.1371/journal.pone.0194459. eCollection 2018.

Abstract

Vitellogenesis is the process of yolk formation via accumulating vitellin (Vn) with nutrients in the oocytes. Expression of vitellogenin (Vg), the precursor of Vn, is one of the indicators for the start of vitellogenesis. In Pacific white shrimp (Litopenaeus vannamei), the type-II vitellogenesis-inhibiting hormone (VIH-2) effectively suppresses hepatopancreatic Vg mRNA expression. In this study, we demonstrate the increasing transcript levels of hepatopancreatic Vg during L. vannamei ovarian development, suggesting that the hepatopancreas-derived Vg/Vn may also contribute to vitellogenesis in this species. Using a combination of in vivo injections and in vitro primary cell cultures, we provide evidences that the inhibition of VIH-2 on hepatopancreatic Vg gene expression is mediated through a functional coupling of the GC/cGMP pathway with different MAPK-dependent cascades in female shrimp. In VIH-2 signaling, the NO-independent GC/cGMP/PKG cascades were upstream of the MAPKs. Activations of the MAPK signal by VIH-2 include the phosphorylation of JNK and the mRNA/protein expression of P38MAPK. Additionally, the cAMP/PKA pathway is another positive intracellular signal for hepatopancreatic Vg mRNA expression but is independent of its VIH-2 regulation. Our findings establish a model for the signal transduction mechanism of Vg regulation by VIH and shed light on the biological functions and signaling of the CHH family in crustaceans.

摘要

卵黄发生是指通过在卵母细胞中积累卵黄蛋白原(Vn)和营养物质来形成卵黄的过程。卵黄蛋白原(Vg)的表达是卵黄发生开始的标志之一。在凡纳滨对虾(Litopenaeus vannamei)中,Ⅱ型卵黄生成抑制激素(VIH-2)能有效抑制肝胰腺 Vg mRNA 的表达。在本研究中,我们发现在凡纳滨对虾卵巢发育过程中肝胰腺 Vg 的转录水平增加,这表明肝胰腺来源的 Vg/Vn 也可能参与该物种的卵黄发生。通过体内注射和体外原代细胞培养相结合的方法,我们提供了证据表明,VIH-2 对肝胰腺 Vg 基因表达的抑制是通过 GC/cGMP 途径与雌性虾中不同 MAPK 依赖性级联的功能偶联来介导的。在 VIH-2 信号通路中,NO 非依赖性 GC/cGMP/PKG 级联位于 MAPKs 的上游。VIH-2 激活 MAPK 信号包括 JNK 的磷酸化和 P38MAPK 的 mRNA/蛋白表达。此外,cAMP/PKA 途径是肝胰腺 Vg mRNA 表达的另一个正向细胞内信号,但不受其 VIH-2 调节的影响。我们的研究结果为 VIH 调节 Vg 表达的信号转导机制建立了一个模型,并阐明了 CHH 家族在甲壳动物中的生物学功能和信号转导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88d7/5874034/99bd6db322b4/pone.0194459.g001.jpg

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