Caenorhabditis elegans pathways that surveil and defend mitochondria (Nature, 2014, 508:406-410)

報告日期: 2015/04/21
報告時間: 17:10/18:00
報告學生: 黃晟榮(以英文報告)
講評老師: 凌斌
附件下載: 下載[1466-1425857720-1.pdf] 

Caenorhabditis elegans pathways that surveil and defend mitochondria

Ying Liu, Buck S. Samuel, Peter C. Breen, & Gary Ruvkun

Nature 508, 406–410, April 2, 2014

Speaker:黃晟榮                                  Time2015/4/21  17:10

Commentator凌斌老師                        PlaceRoom 602

Abstract

Mitochondria is an important organelle, it has many functions such as production of energy, storage of calcium ion, regulation of the membrane potential, apoptosis-programmed cell death, certain heme synthesis reactions and steroid synthesis. However, mitochondrial function is challenged by toxic by-products of metabolism as well as by pathogen attack1-3. C. elegans normally face to mitochondrial defect by activation of drug-detoxification, mitochondrial repair and pathogen-response pathways. So far, mitochondrial surveillance mechanism is unclear. To identify the molecular basis behind the detection of animal mitochondrial dysfunction and its coupling to a detoxification response, the authors performed a genome-wide RNAi screen for gene inactivation that render C. elegansunresponsive to mitochondrial dysfunction. From genome-wide RNAi screen, they found that mitochondrial surveillance and response was disrupted by 45 gene inactivation.One of the gene inactivation that potently disrupts response to mitochondrial dysfunction, sptl-1, encodes serine palmitoyltransferase, which has a role in the sphingolipid biosynthesis pathway. hmgs-1, which encodes an HMG-CoA synthase of the mevalonate synthetic pathway, is also a strong hit from the genome-wide screen. In this studies have revealed roles of ceramide and mevalonate in mitochondrial surveillance.

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