近期發(fā)表在Journal of Dental Research上的一篇關(guān)于表觀遺傳學(xué)在口腔生物學(xué)中的意義的綜述報(bào)道,。遺傳信息的編碼不僅取決于線性的DNA序列,，而且還會(huì)經(jīng)染色質(zhì)結(jié)構(gòu)進(jìn)行表觀遺傳學(xué)修改,，如DNA甲基化和與DNA結(jié)合蛋白的共價(jià)修飾,。這些“表觀遺傳學(xué)”可以通過改變?nèi)旧|(zhì)的結(jié)構(gòu)來影響基因的表達(dá),。自然發(fā)生的甲基化通常在CpG序列的胞嘧啶堿基上,，他參與了基因正確表達(dá)的控制,。
DNA甲基化通常與組蛋白脫乙?；⑷旧|(zhì)濃縮和基因沉默相關(guān),，染色質(zhì)濃縮,，和基因沉默。不同的甲基化可引起不同的組織模式和疾病差異,。這種甲基化可變位點(diǎn)并非均勻分布在整個(gè)基因組,，而是集中在某些基因，這些基因進(jìn)行基因轉(zhuǎn)錄,、生長,、代謝,、分化和癌變的調(diào)控。甲基化狀態(tài)可產(chǎn)生表觀遺傳學(xué)改變,。環(huán)境壓力包括有毒物質(zhì),，以及微生物和病毒的接觸，也可以改變表觀遺傳學(xué),，從而改變基因活化和細(xì)胞表型,。由于DNA甲基化往往是繼隨與細(xì)胞分裂，甲基化可變位點(diǎn)的積累,，并隨著時(shí)間的推移可能會(huì)導(dǎo)致細(xì)胞代謝穩(wěn)態(tài),、對(duì)刺激的反應(yīng)等持續(xù)的改變，或者會(huì)保留的異常表型,。因此,， DNA的表觀遺傳學(xué)依然是遺傳、疾病和環(huán)境之間主要和以前缺少研究的環(huán)節(jié),?？谇簧飳W(xué)面臨的挑戰(zhàn)是加強(qiáng)這種機(jī)制的理解，確定表觀遺傳學(xué)在疾病發(fā)病機(jī)制或治療響應(yīng)的作用,。（生物谷Bioon.com）
生物谷推薦原始出處：
Journal of Dental Research, Vol. 88, No. 5, 400-408 (2009) DOI: 10.1177/0022034509335868
Epigenetics: Connecting Environment and Genotype to Phenotype and Disease
S.P. Barros* and S. Offenbacher
Center for Oral and Systemic Diseases, Department of Periodontology, School of Dentistry, University of North Carolina at Chapel Hill, Room 222, CB 7455, Chapel Hill, NC, USA 27599
Genetic information is encoded not only by the linear sequence of DNA, but also by epigenetic modifications of chromatin structure that include DNA methylation and covalent modifications of the proteins that bind DNA. These "epigenetic marks" alter the structure of chromatin to influence gene expression. Methylation occurs naturally on cytosine bases at CpG sequences and is involved in controlling the correct expression of genes. DNA methylation is usually associated with triggering histone deacetylation, chromatin condensation, and gene silencing. Differentially methylated cytosines give rise to distinct patterns specific for each tissue type and disease state. Such methylation-variable positions (MVPs) are not uniformly distributed throughout our genome, but are concentrated among genes that regulate transcription, growth, metabolism, differentiation, and oncogenesis. Alterations in MVP methylation status create epigenetic patterns that appear to regulate gene expression profiles during cell differentiation, growth, and development, as well as in cancer. Environmental stressors including toxins, as well as microbial and viral exposures, can change epigenetic patterns and thereby effect changes in gene activation and cell phenotype. Since DNA methylation is often retained following cell division, altered MVP patterns in tissues can accumulate over time and can lead to persistent alterations in steady-state cellular metabolism, responses to stimuli, or the retention of an abnormal phenotype, reflecting a molecular consequence of gene-environment interaction. Hence, DNA epigenetics constitutes the main and previously missing link among genetics, disease, and the environment. The challenge in oral biology will be to understand the mechanisms that modify MVPs in oral tissues and to identify those epigenetic patterns that modify disease pathogenesis or responses to therapy.
