果蠅去頭蓋蛋白質2 對果蠅卵發育過程中軸向之調控分析

Abstract

在酵母和人類的系統中,去頭蓋蛋白已被充分研究。研究發現Dcp1會和Dcp2 形成 heterodimer, 此酵素複合體具有去除訊息RNA頭蓋之活性。Dcp2是去頭蓋作用的催化中心, 且Dcp1被認為能增進其活性。另外, 越來越多的證據顯示許多蛋白質亦參與在此複合體中。Dcp1 和 Dcp2 的另一個特徵是他們會與 Xrn1 , Edc3 和 Dhh1 這些參與在訊息RNA降解路徑上的成員共同在細胞質內形成聚集點, 這個特殊的結構被稱作 P body ,且被認為是訊息 RNA 被進行降解的地點。 我們的之前的研究發現果蠅去頭蓋蛋白 1, dDcp1, 是 oskar mRNP的一個成員且和其定位於卵後端有關 (Lin et al., 2006)。 dDcp1突變時會造成果蠅胚胎腹節發育缺失, 此外, 其他 oskar mRNP 的成員的正確定位亦受到破壞, 如Exu , Yps 以及Orb. 這個發現揭示了訊息RNA在定位 ,轉錄, 轉譯和降解中間的緊密連接的可能性。 經過果蠅基因體比對, 我們找到了唯一可能的 dDcp2 基因, CG6169 。我們分析 dDcp2 突變對偶基因, BG1766, dDcp2de21,發現兩個突變對偶基因都造成前後及背腹的發育缺失。而這些特殊的性狀可能是 Osk, Stau 和 Vasa 蛋白沒能正確座落至卵後端所致。 另一個有趣的發現是當 dDcp2 基因被刪除時, 果蠅卵室內之護理細胞 (nurse cell)內, 可能的 P body 結構會發生明顯的放大和累積, 這也許是訊息RNA 降解路徑受阻的結果。

Decapping complex in yeast and human systems are well studied. It is reported that Dcp1 and Dcp2 form a heterodimer with decapping activity. Dcp2 is the catalytic center of decapping process and Dcp1 is believed to promote the decapping activity. And increasing lines of evidence show that many proteins may be associated in the decapping complex. Another distinct feature of Dcp1 and Dcp2 is their colocalization within cytoplasmic foci associated with other mRNA degradation components such as Xrn1, Edc3 and Dhh1. This specialized structure is called processing body (P body) which is referred to as the sites for mRNA degradation. Our previous research uncovered Drosophila decapping protein 1,dDcp1, is a novel component of oskar mRNP complex and directs its posterior localization in the oocyte. (Lin et al., 2006b) dDcp1 mutant causes posterior group phenotype. And dDcp1 is also required for the proper posterior localization of other oskar mRNP complex component, such as Exu, Yps, and Orb. This discovery reveals the possibility of close linkage among transportation, transcription, translation and degradation. According to the Drosophila genome wide gene BLAST result, we uncovered the putative and unique dDcp2 gene, CG6169. We analyzed the dDcp2 mutant allele, BG1766, and dDcp2 null allele, dDcp2de21. Both mutant alleles cause anterior- posterior and dorsal-ventral patterning defect. And the distinct phenotype could be the consequence of mislocalization of Osk, Stau and Vasa proteins. The other interesting finding is that deletion of dDcp2 gene causes the enlargement and accumulation of P body-like structure, which may be the result of the mRNA decay pathway deficiency.