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果蝇 InsP3 受体突变体幼虫中基因表达的模式揭示了 InsP3 信号在碳水化合物和能量代谢中的作用。

Patterns of gene expression in Drosophila InsP3 receptor mutant larvae reveal a role for InsP3 signaling in carbohydrate and energy metabolism.

机构信息

National Centre for Biological Sciences, Tata Institute of Fundamental Research, Bangalore, Karnataka, India.

出版信息

PLoS One. 2011;6(8):e24105. doi: 10.1371/journal.pone.0024105. Epub 2011 Aug 25.

DOI:10.1371/journal.pone.0024105
PMID:21901161
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3162032/
Abstract

BACKGROUND

The Inositol 1,4,5-trisphosphate receptor (InsP(3)R) is an InsP(3) gated intracellular Ca(2+)-release channel. Characterization of Drosophila mutants for the InsP(3)R has demonstrated that InsP(3)-mediated Ca(2+) release is required in Drosophila larvae for growth and viability.

METHODOLOGY/PRINCIPAL FINDINGS: To understand the molecular basis of these growth defects a genome wide microarray analysis has been carried out with larval RNA obtained from a strong InsP(3)R mutant combination in which 1504 independent genes were differentially regulated with a log(2) of fold change of 1 or more and P<0.05. This was followed by similar transcript analyses from InsP(3)R mutants where growth defects were either suppressed by introduction of a dominant suppressor or rescued by ectopic expression of an InsP(3)R transgene in the Drosophila insulin like peptide-2 (Dilp2) producing cells.

CONCLUSIONS/SIGNIFICANCE: These studies show that expression of transcripts related to carbohydrate and amine metabolism is altered in InsP(3) receptor mutant larvae. Moreover, from a comparative analysis of genes that are regulated in the suppressed and rescued conditions with the mutant condition, it appears that the organism could use different combinations of pathways to restore a 'normal' growth state.

摘要

背景

肌醇 1,4,5-三磷酸受体（InsP(3)R）是一种 InsP(3)门控细胞内 Ca(2+)释放通道。对果蝇 InsP(3)R 突变体的研究表明，InsP(3)介导的 Ca(2+)释放对于果蝇幼虫的生长和存活是必需的。

方法/主要发现：为了了解这些生长缺陷的分子基础，我们对来自于 InsP(3)R 强突变体组合的幼虫 RNA 进行了全基因组微阵列分析，其中 1504 个独立基因的表达发生了差异调节，对数（2）的倍数变化为 1 或更多，P<0.05。随后，我们对 InsP(3)R 突变体进行了类似的转录分析，在这些突变体中，生长缺陷要么通过引入显性抑制子而得到抑制，要么通过在产生胰岛素样肽-2 (Dilp2)的果蝇中异位表达 InsP(3)R 转基因而得到挽救。

结论/意义：这些研究表明，InsP(3)受体突变体幼虫中与碳水化合物和胺代谢相关的转录本表达发生了改变。此外，通过对抑制和挽救条件下与突变条件下受调控基因的比较分析，似乎生物体可以使用不同的途径组合来恢复“正常”的生长状态。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e75f/3162032/b030f77f868b/pone.0024105.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e75f/3162032/d2b3b2e92043/pone.0024105.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e75f/3162032/0c2eec493649/pone.0024105.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e75f/3162032/d7aed9e7212e/pone.0024105.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e75f/3162032/0a4b30f27b00/pone.0024105.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e75f/3162032/a8f7a1cb9675/pone.0024105.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e75f/3162032/f9b4489525b9/pone.0024105.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e75f/3162032/b030f77f868b/pone.0024105.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e75f/3162032/d2b3b2e92043/pone.0024105.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e75f/3162032/0c2eec493649/pone.0024105.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e75f/3162032/d7aed9e7212e/pone.0024105.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e75f/3162032/0a4b30f27b00/pone.0024105.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e75f/3162032/a8f7a1cb9675/pone.0024105.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e75f/3162032/f9b4489525b9/pone.0024105.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e75f/3162032/b030f77f868b/pone.0024105.g007.jpg

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