近日，国际著名杂志PLoS One在线刊登了巴西研究人员的最新研究成果“Trypanosoma cruzi Gene Expression in Response to Gamma Radiation，”，文章中，作者通过研究揭示了克鲁斯锥虫面对电离辐射有害压力时如何来改变自身的基因表达，从而来应对这种有害压力。
克鲁斯锥虫是一种引起美洲锥虫病的病原体，这种病原体对电离辐射导致的DNA损伤有高度抗性，一种可能性是，接受500Gy单位的γ射线辐射后，这种病原体能够启动自身的DNA双链修复程序对断裂DNA进行修复，48小时之内便可以使染色体链得到修复。科学家曾经将时程研究应用于酵母、拟南芥、古细菌、人类成纤维细细胞以及耐辐射球菌中，研究它们应对γ射线时总体基因的表达，可是对于克鲁斯锥虫应对电离辐射却研究的比较少，尤其是在面对γ射线辐射时，克鲁斯锥虫进行DNA修复和细胞恢复时基因表达的变化上研究的比较少。
文章中，Priscila Grynberg等运用时程微点阵分析的方法，对于辐射后的克鲁斯锥虫标出了273个基因表达发生明显变化的基因，这些表达发生变化的基因可以分为四类：编码未知功能蛋白的基因；编码假设蛋白的基因；编码retrotransposon hot spot（RHS）的基因以及一些无用的序列，60%以上的基因都是编码未知功能蛋白的上调基因，其余的上调基因包括RHS和无用的一些序列，作者的研究揭示克鲁斯锥虫基因的转录并不是依靠操纵子单位，而是依靠多顺反子单位来进行转录，在作者的研究中，他们发现了一个DNA双链破碎修复过程的基因，该基因也是上调的，编码酪胺酰基-DNA磷酸二酯酶，这篇文章，作者阐释了克鲁斯锥虫在应对电路辐射时的特殊应对机制，从而为后期的科学研究中提出了很多有意思的问题，在面对危害压力时，有机体如何改变自身的基因表达来躲避这种危害。（生物谷：T.Shen编译）
doi:10.1371/journal.pone.0029596
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Trypanosoma cruzi Gene Expression in Response to Gamma Radiation
Priscila Grynberg1, Danielle Gomes Passos-Silva1, Marina de Moraes Mourão3,5, Roberto Hirata Jr4, Andrea Mara Macedo1, Carlos Renato Machado1, Daniella Castanheira Bartholomeu2, Glória Regina Franco1*
Trypanosoma cruzi is an organism highly resistant to ionizing radiation. Following a dose of 500 Gy of gamma radiation, the fragmented genomic DNA is gradually reconstructed and the pattern of chromosomal bands is restored in less than 48 hours. Cell growth arrests after irradiation but, while DNA is completely fragmented, RNA maintains its integrity. In this work we compared the transcriptional profiles of irradiated and non-irradiated epimastigotes at different time points after irradiation using microarray. In total, 273 genes were differentially expressed; from these, 160 were up-regulated and 113 down-regulated. We found that genes with predicted functions are the most prevalent in the down-regulated gene category. Translation and protein metabolic processes, as well as generation of precursor of metabolites and energy pathways were affected. In contrast, the up-regulated category was mainly composed of obsolete sequences (which included some genes of the kinetoplast DNA), genes coding for hypothetical proteins, and Retrotransposon Hot Spot genes. Finally, the tyrosyl-DNA phosphodiesterase 1, a gene involved in double-strand DNA break repair process, was up-regulated. Our study demonstrated the peculiar response to ionizing radiation, raising questions about how this organism changes its gene expression to manage such a harmful stress.
