中科院上海生命科学研究院上海交通大学医学院健康科学研究所分子遗传实验室殷善叶博士等，在孔祥银研究员的指导下，与巴斯大学教授Hurst合作，通过整合大规模芯片数据和生物信息学分析，发现X染色体基因表达噪音并不比常染色体高；而常染色单拷贝表达的基因的确具有较高的噪音。逃脱失活并不会为这些X染色体基因带来更高的表达丰度或表达噪音。 他们进一步发现基因表达丰度是决定表达噪音的重要因素；升高表达水平能降低基因的表达噪音。
X染色体通过剂量补偿机制，达到和常染色体相似的基因表达丰度。该工作首次发现了X染色体不仅基因表达剂量存在补偿，其表达噪音也得到了 “补偿”；并提出单拷贝的X染色体基因表达剂量补偿在一定程度上是为了降低其有害的基因表达噪音。这一研究结果在线发表在2009年的Genome Biology杂志上。
该项工作得到了科技部、国家自然科学基金委和中科院项目的支持。（生物谷Bioon.com）
生物谷推荐原始出处：
Genome Biology 2009, 10:R74doi:10.1186/gb-2009-10-7-r74
Dosage compensation on the active X chromosome minimizes transcriptional noise of X-linked genes in mammals
Shanye Yin , Ping Wang , Wenjun Deng , Hancheng Zheng , Landian Hu , Laurence D Hurst and Xiangyin Kong
Background
Theory predicts that haploid-expressed genes should have noisier expression than comparable diploid-expressed ones with the same expression level. However, in mammals there are several classes of gene that are monoallelically-expressed, including X-linked genes, imprinted genes and some other autosomal genes. Does it follow that the evolution of X chromosomes in eukaryotes comes at the cost of increased transcriptional noise in the heterogametic sex? Moreover, is X-inactivation in mammalian females associated with an increase in transcriptional variation? To address these questions, we analyze gene expression variation between replicate samples of diverse mammalian cell lines in steady-state using microarray data.
Results
We observe that transcriptional variation of X-linked genes is no different to that of autosomal genes both before and after control for transcript abundance. By contrast, autosomal genes subject to allelic exclusion do have unusually high noise levels even allowing for their low transcript abundance. The prior theory we suggest was insufficient, at least as regards X-chromosomes, as it failed to appreciate the regulatory complexity of gene expression, not least the effects of genomic neighbourhood.
Conclusions
These results suggest that high noise is not a necessary consequence of haploid expression and emphasize the primacy of expression level as a determinant of noise. The latter has consequences for understanding the etiology of haplo-insufficiency and the evolution of gene expression levels. Given the coupling between expression level and noise on the X-chromosome, we suggest that part of the selective advantage of dosage compensation is noise abatement of X-linked genes.
