Abstract
The genetically amenable organism Drosophila melanogaster has been estimated to have 14,076 protein coding genes in the genome, according to the flybase release note R5.13 (http://flybase.bio.indiana.edu/static_pages/docs/release_notes.html). Recent application of RNA interference (RNAi) to the study of developmental biology in Drosophila has enabled us to carry out a systematic investigation of genes affecting various specific phenotypes. In order to search for genes supporting cell survival, we conducted an immunohistochemical examination in which the RNAi of 2,497 genes was independently induced within the dorsal compartment of the wing imaginal disc. Under these conditions, the activities of a stress-activated protein kinase JNK (c-Jun N-terminal kinase) and apoptosis-executing factor Caspase-3 were monitored. Approximately half of the genes displayed a strong JNK or Caspase-3 activation when their RNAi was induced. Most of the JNK activation accompanied Caspase-3 activation, while the opposite did not hold true. Interestingly, the area activating Caspase-3 was more broadly seen than that activating JNK, suggesting that JNK is crucial for induction of non-autonomous apoptosis in many cases. Furthermore, the RNAi of essential factors commonly regulating transcription and translation showed a severe and cell-autonomous apoptosis but also elicited another apoptosis at an adjacent area in a non-autonomous way. We also found that the frequency of apoptosis varies depending on the tissues.
Highlights
Mechanisms controlling apoptosis have been extensively studied, and various factors are known to be involved in the intrinsic and extrinsic apoptotic pathways.[1,2,3,4]. These pathways play a pivotal role in the execution of most cases of apoptosis, the apoptosis shown in developing animal tissues is affected by various growth and differentiation signals to promote or repair organ development.[5]
Caspase-3 plays a central role in most apoptosis, while JNK leads to a subgroup of stress-induced apoptosis.[18]
In the Drosophila wing disc, JNK activation is usually linked to the activation of Caspase-3.16 Puc is a protein phosphatase inactivating JNK, and its transcription occurs in response to the JNK signal, thereby making a negative-regulatory circuit.[19]
Summary
Mechanisms controlling apoptosis have been extensively studied, and various factors are known to be involved in the intrinsic and extrinsic apoptotic pathways.[1,2,3,4] these pathways play a pivotal role in the execution of most cases of apoptosis, the apoptosis shown in developing animal tissues is affected by various growth and differentiation signals to promote or repair organ development.[5]. In order to systematically investigate the apoptosis phenotype caused by reducing each gene function in the developing animal tissues, we employed a genetically amenable fruit fly Drosophila melanogaster, in which each gene can be knocked down by RNAi,[12,13,14] to observe the effect on apoptosis induction. Loss of membrane proteins frequently caused JNK activation, which had been expected because cell-cell communication is presumed to be important for many developmental processes, including apoptosis in multicellular organisms. These results, as well as the database showing the immunofluorescent data, provide an archival source for survey of genes and for fine analysis of each gene in apoptosis regulation using the Drosophila imaginal discs
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