Proteome analysis on lethal effect of l (2) in the sex-linked balanced lethal strains of silkworm, Bombyx mori

文献类型： 外文期刊

第一作者： Chen, Jine

作者： Chen, Jine;Zhong, Boxiong;Chen, Jine;Niu, Baolong;Wang, Yongqiang;Liu, Yan;Liu, Peigang;Meng, Zhiqi

作者机构：

关键词： embryo;2-DE;MALDI-TOF/TOF;sex-linked balanced lethal;silkworm

期刊名称：BIOTECHNOLOGY AND BIOPROCESS ENGINEERING （ 影响因子：2.836； 五年影响因子：2.281 ）

ISSN： 1226-8372

年卷期： 2012 年 17 卷 2 期

页码：

收录情况： SCI

摘要： The sex-linked balanced lethal (SLBL) strains of silkworm serve as an effective system for sex-control in silkworm. To gain comprehensive insight into the effect of one sex-linked balanced lethal gene l(2), comparative proteomic analysis was carried out between the survival embryos (W(+l1)Z(l1+l2)) and lethal embryos (W(+l1)Z(+l1l2)) before the lethal stage. The lethal stage of l(2) was confirmed by observing the typical dead embryo morphology. The two genotype embryos before lethal stage were distinguished using polymorphic simple sequence repeats (SSR) markers closely linked to l(2) on the sex chromosome. Finally, 11 differentially expressed protein spots were successfully identified by MALDI-TOF/TOF mass spectrometry (MS). Among them, only 1 protein identified as heat shock protein 20.4 (HSP20.4) was up-regulated in the lethal embryos, while the other 10 were down-regulated. The up-regulation of HSP20.4 suggests that there may be abnormal polypeptides produced in the lethal embryos. The gene ontology (GO) annotation indicated those down-regulated proteins are involved in important biological processes including embryo development, nucleoside metabolism, tRNA splicing, translation and protein folding. The biological pathway analysis showed that those down-regulated proteins are mainly involved in spindle assemblage and morphogenesis. Based on our results, we suggest that the l(2) may be the mutant expressing abnormal polypeptides. Its expression has a negative effect on mitosis and morphogenesis processes. The death of the embryos may be caused by the accumulation of abnormal polypeptides and the handicap of cell proliferation and morphogenesis.

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