Transcriptional regulation of a metastasis suppressor gene by Tip60 and beta-catenin complexes

Defining the molecular strategies that integrate diverse signalling pathways in the expression of specific gene programmes that are critical in homeostasis and disease remains a central issue in biology. This is particularly pertinent in cancer biology because downregulation of tumour metastasis suppressor genes is a common occurrence, and the underlying molecular mechanisms are not well established. Here we report that the downregulation of a metastasis suppressor gene, KAI1, in prostate cancer cells involves the inhibitory actions of beta-catenin, along with a reptin chromatin remodelling complex. This inhibitory function of beta-catenin-reptin requires both increased beta-catenin expression and recruitment of histone deacetylase activity. The coordinated actions of beta-catenin-reptin components that mediate the repressive state serve to antagonize a Tip60 coactivator complex that is required for activation; the balance of these opposing complexes controls the expression of KAI1 and metastatic potential. The molecular mechanisms underlying the antagonistic regulation of beta-catenin-reptin and the Tip60 coactivator complexes for the metastasis suppressor gene, KAI1, are likely to be prototypic of a selective downregulation strategy for many genes, including a subset of NF-kappaB target genes.     

Epigenetic silencers and Notch collaborate to promote malignant tumours by Rb silencing

Cancer is both a genetic and an epigenetic disease. Inactivation of tumour-suppressor genes by epigenetic changes is frequently observed in human cancers, particularly as a result of the modifications of histones and DNA methylation. It is therefore important to understand how these damaging changes might come about. By studying tumorigenesis in the Drosophila eye, here we identify two Polycomb group epigenetic silencers, Pipsqueak and Lola, that participate in this process. When coupled with overexpression of Delta, deregulation of the expression of Pipsqueak and Lola induces the formation of metastatic tumours. This phenotype depends on the histone-modifying enzymes Rpd3 (a histone deacetylase), Su(var)3-9 and E(z), as well as on the chromodomain protein Polycomb. Expression of the gene Retinoblastoma-family protein (Rbf) is downregulated in these tumours and, indeed, this downregulation is associated with DNA hypermethylation. Together, these results establish a mechanism that links the Notch-Delta pathway, epigenetic silencing pathways and cell-cycle control in the process of tumorigenesis.     

AhHDA1影响花生毛状根生长的研究

花生组蛋白去乙酰化酶AhHDA1转到花生毛状根中超表达后,短侧根的毛状根比例增加. 基因表达检测结果显示,AhHDA1超表达后上调了细胞周期相关基因AhCYCD4和生长素信号转导相关基因AhIAA28的表达水平,而AhARF19的表达水平被显著抑制. 进一步通过LUC实验发现, AhHDA1激活AhCYCD4和AhIAA28启动子的活性. 说明AhHDA1可能通过调控生长素信号转导和细胞分裂影响花生毛状根侧根的生长.     

红砂促分裂原活化蛋白激酶MAPK基因cDNA片段克隆及序列分析

研究了参与非生物胁迫的促分裂原活化蛋白激酶MAPK基因在红砂抗旱中的作用.通过实验克隆得到了红砂MAPK基因550 bp的cDNA片段,与已知的植物MAPK基因的相应片段表现出较高的同源性(最高达80.5%).MAPK基因在红砂叶片和茎中无组织特异性表达,且随着干旱胁迫程度的加剧其表达量增加,说明MAPK基因在红砂抗旱中起重要作用.     

Chromosomal landscape of nucleosome-dependent gene expression and silencing in yeast

Eukaryotic genomes are packaged into nucleosomes, which are thought to repress gene expression generally. Repression is particularly evident at yeast telomeres, where genes within the telomeric heterochromatin appear to be silenced by the histone-binding silent information regulator (SIR) complex (Sir2, Sir3, Sir4) and Rap1 (refs 4-10). Here, to investigate how nucleosomes and silencing factors influence global gene expression, we use high-density arrays to study the effects of depleting nucleosomal histones and silencing factors in yeast. Reducing nucleosome content by depleting histone H4 caused increased expression of 15% of genes and reduced expression of 10% of genes, but it had little effect on expression of the majority (75%) of yeast genes. Telomere-proximal genes were found to be de-repressed over regions extending 20 kilobases from the telomeres, well beyond the extent of Sir protein binding and the effects of loss of Sir function. These results indicate that histones make Sir-independent contributions to telomeric silencing, and that the role of histones located elsewhere in chromosomes is gene specific rather than generally repressive.     

NaCl和Na2CO3胁迫下的高粱MAPKs基因家族表达模式

通过在全基因组水平上进行NaCl和Na2CO3胁迫下高粱MAPKs基因表达模式的研究, 探索高粱MAPKs基因在胁迫条件下参与信号传导的机理. 结果
表明, 从高粱基因组中鉴定出16个MAPKs基因, 命名为SbMPKs. 这些SbMPKs在NaCl和Na2CO3胁迫下的表达模式明显不同, 表明中性盐胁迫诱导的信号响应不同于碱性盐. 在NaCl胁迫下, 除了SbMPK13的表达量在12 h时达到最大值外, 所有高粱MAPKs基因在24 h内表达持续上调; 在Na2CO3胁迫下, 只有SbMPK3,SbMPK10和SbMPK13表达上调, 表明这3个基因可能与高粱碱性盐胁迫应答反应有关. 系统发育分析表明, SbMPK13属于C组MAPKs基因, 并且与水稻中受脱落酸（ABA）和盐胁迫诱导表达的OsMAPK2亲缘关系较近, 进一步证实了SbMPK13可能是参与高粱盐胁迫应答的重要调控基因.     

TSA对花生响应干旱过程中光合特性及相关基因表达的影响

以粤油7号和汕优523两个不同抗旱性品种花生材料,研究组蛋白去乙酰化酶抑制剂曲古抑菌素A（Trichostatin A,TSA）在模拟干旱条件下对花生幼苗叶片为叶绿素含量、荧光特性和光合相关基因表达的影响. 结果表明:粤油7号的总电子传递速率（ETR）和PSⅡ光量子产率（PSⅡ）对干旱的响应较汕优523强,1 mol/L TSA处理12 h能使2个品种的花生在干旱条件下保持较高的光合效率;经TSA处理的的花生在干旱胁迫下,叶片AhLHCB3和AhPORA基因表达上调,AhRUBP基因表达下调,差异均有统计学意义（P0.05）,2种不同抗旱性品种花生在TSA影响下对干旱的响应趋势是一致的,幅度和响应时间有差异.