結晶毒素[Crystal(Cry) toxins]是由革蘭氏陽性桿菌[Bacillus thuringiensis(Bt)]蘇利桿菌所產生的膜穿孔毒素[Pore-forming toxins (PFTs)]。膜穿孔毒素可在宿主細胞膜上形成孔洞進而使宿主細胞死亡，在許多人類病原菌當中，膜穿孔毒素是很重要的一種致病毒理因子。Cry毒素由於對昆蟲與線蟲類的特殊專一性，而被廣泛應用在生物防治上。在過去文獻已經指出Cry毒素的其中一員Cry5B，可以毒殺許多種類的線蟲，包含實驗室常用的模式生物線蟲(C. elegans) ，藉此我們進行Cry5B和線蟲之間的膜穿孔毒素—宿主交互作用之相關研究。
我們利用全基因體微晶片進行處理Cry5B後線蟲之基因轉錄體分析，發現其中sir-2.3基因的轉錄在處理Cry5B後有顯著的上調現象。SIR-2.3是需要菸鹼醯胺腺嘌呤二核苷酸(NAD)的去乙醯酵素並且是SIR2家族的一員，在過去已有研究指出SIR-2.3的哺乳類同源物SIRT4，可以抑制胰臟細胞胰島素的分泌。在本研究中我們發現SIR-2.3與類胰島素受器DAF-2在線蟲抵抗Cry5B的毒殺當中都扮演了很重要的角色，我們另外也去探討SIR-2.3與DAF-2兩者之間的關係。

Pore-Forming toxins(PFTs) are bacterial toxins that form holes at the plasma membrane of cells and play important roles in the pathogenesis of many important human pathogens. Crystal(Cry) toxin is one type of the PFTs produced by Bacillus thuringiensis(Bt), and is also the most widely used natural insecticides in agriculture for many decades. It has been reported that C. elegans and other nematodes can be intoxicated and killed by the three-domain Bt Cry toxins, including Cry5B in this study.
Characterizations of the mode of action of Cry5B in C. elegans may pave the way for understanding the PFT-host interactions in vivo.
From our previous microarray data, we found significant transcriptional upregulation of the sir-2.3 gene after Cry5B treatment in
C. elegans. SIR-2.3 is a member of the SIR2 family proteins with a NAD-dependent histone deacetylase activity. We have demonstrated that DAF-2 insulin-like signaling pathway was important for the intrinsic
cellular defense against PFTs. Interestingly, it has been reported that the mammalian SIR-2.3 homolog, SIRT4, can also inhibit the insulin secretion in pancreatic  cells. Our current data suggested that sir-2.3 and daf-2 all function in Cry5B intoxication, and we also analyzed the
interaction between these two genes.

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