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Gregis V Sessa A Colombo L Kater MM 《The Plant journal : for cell and molecular biology》2008,56(6):891-902
The formation of flowers starts when floral meristems develop on the flanks of the inflorescence meristem. In Arabidopsis the identity of floral meristems is promoted and maintained by APETALA1 (AP1) and CAULIFLOWER (CAL). In the ap1 cal double mutant the meristems that develop on the flanks of the inflorescence meristem are unable to establish floral meristem identity and develop as inflorescence meristems on which new inflorescence meristems subsequently proliferate. We demonstrate in contrast to previous models that AGAMOUS-LIKE 24 (AGL24) and SHORT VEGETATIVE PHASE (SVP) are also floral meristem identity genes since the ap1-10 agl24-2 svp-41 triple mutant continuously produces inflorescence meristems in place of flowers. Furthermore, our results explain how AP1 switches from a floral meristem identity factor to a component that controls floral organ identity. 相似文献
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棉花MADS框蛋白基因(GhMADS1)的克隆 总被引：3，自引：0，他引：3
作为转录因子,MADS框蛋白基因在植物花器官发育中有着重要的功能。为研究棉花花器官发育的分子机理,以棉花花器官突变体CHV1(cotton homeotic variant)和徐州142正常植株为材料,利用棉花EST数据库资料,通过EST序列整合,从陆地棉徐州142花蕾中克隆出一个MADS框蛋白的编码区段,GenBank登录号为AF538965。该片段(GhMADS1)长713bp,包含一个711bp的开放阅读框,推导的氨基酸序列(236个氨基酸)与葡萄、烟草、矮牵牛、拟南芥和金鱼草等的AGL2组MADS框蛋白有很高的序列相似性。系统进化分析同样将GhMADS1基因归人AGt2组MADS框蛋白。RT-PCR分析显示,该基因在陆地棉的花瓣、雄蕊、胚珠和纤维中表达,特别是在花瓣中表达量最高,而在根、茎、叶等营养器官和棉花同源异型突变体CHV1(所有花器官均变为苞叶状叶性器官)的变异花蕾中不表达。这些结果说明GhMADS1基因可能在棉花花器官发育中有着重要的功能。 相似文献
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为了考察小鼠(Mus musculus)孤雌激活胚胎H3K27三甲基化模式与体内正常胚胎之间的差异,以及曲古抑菌素A(TSA)对孤雌胚H3K27三甲基化水平的影响,探究表观遗传修饰对孤雌胚胎发育的作用。首先,用H3K27me3特异性抗体对MⅡ期卵母细胞染色,利用激光共聚焦对其荧光强度进行检测,结果发现该时期的甲基化荧光强度相对较低。接着,采用同样的方法对小鼠孤雌胚胎和体内正常胚胎植入前各时期的H3K27me3模式进行比较,结果显示,从2-细胞到囊胚期孤雌组呈现逐渐升高的趋势,与体内组变化趋势完全相反,且总体平均荧光强度较体内组普遍偏低。孤雌胚胎经TSA处理后,处理组和未处理组在前三个时期虽然没有显著性差异(P0.05),但是处理之后的H3K27三甲基化水平有所提高,囊胚期与未处理组相比有显著性差异(P0.05)。以上结果表明,小鼠孤雌胚胎的H3K27三甲基化模式与体内胚胎之间存在着巨大的差异,这可能是造成孤雌胚胎发育能力差的重要原因之一。TSA处理对H3K27me3模式造成了一定的影响,使体外培养环境有所改善,这可能对提高孤雌胚胎发育能力具有一定的意义。 相似文献
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Orchids are known for their beauty and complexity of flower and ecological strategies. The evolution in orchid floral morphology, structure, and physiological properties has held the fascination of botanists for centuries, from Darwin through to the present. In floral studies, MADS‐box genes contributing to the now famous ABCDE model of floral organ identity control have dominated conceptual thinking. The sophisticated orchid floral organization offers an opportunity to discover new variant genes and different levels of complexity to the ABCDE model. Recently, several remarkable research reports on orchid MADS‐box genes, especially B‐class MADS‐box genes, have revealed the evolutionary track and important functions on orchid floral development. Diversification and fixation of both paleoAP3 gene sequences and expression profiles might be explained by subfunctionalization and even neofunctionalization. Knowledge about MADS‐box genes encoding ABCDE functions in orchids will give insights into the highly evolved floral morphogenetic networks of orchids. 相似文献
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The inflorescence meristem produces floral primordia that remain undifferentiated during the first stages of flower development. Genes controlling floral meristem identity include LEAFY (LFY), APETALA1 (AP1), CAULIFLOWER (CAL), LATE MERISTEM IDENTITY 1 (LMI1), SHORT VEGETATIVE PHASE (SVP) and AGAMOUS-LIKE24 (AGL24). The lfy mutant shows partial reversions of flowers into inflorescence shoot-like structures and this phenotype is enhanced in the lfy ap1 double mutant. Here we show that combining the lfy mutant with agl24 and svp single mutants or with the agl24 svp double mutant enhances the lfy phenotype and that the lfy agl24 svp triple mutant phenocopies the lfy ap1 double mutant. Analysis of the molecular interactions between LFY, AGL24 and SVP showed that LFY is a repressor of AGL24 and SVP, whereas LMI1 is a positive regulator of these genes. Moreover, AGL24 and SVP positively regulate AP1 and LFY by direct binding to their regulatory regions. Since all these genes are important for establishing floral meristem identity, regulatory loops are probably important to maintain the correct relative expression levels of these genes. 相似文献
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Yong‐Yan Bi Gang Shen Yong Quan Wei Jiang Fulin Xu 《Journal of cellular physiology》2018,233(11):8896-8907
Gliomas are the commonest and most aggressive primary malignant tumor in the central nervous system. Long noncoding RNAs (lncRNAs) have been identified to act as crucial regulators in multiple biological processes, including tumorigenesis. FAM83H antisense RNA1 (FAM83H‐AS1) has been uncovered to be dysregulated in several cancers. However, the biological role of FAM83H‐AS1 in glioma still needs to be investigated. Currently, our findings indicated that FAM83H‐AS1 was upregulated in glioma tissues and cell lines and high level of FAM83H‐AS1 was associated with poor prognosis of glioma. Loss‐of‐function assays demonstrated that silenced FAM83H‐AS1 obviously suppressed cell proliferation via regulating the cell‐cycle distribution and cell apoptosis rate, and mechanistic experiments revealed that FAM83H‐AS1 could epidemically silence CDKN1A expression through recruiting EZH2 to the promoter of CDKN1A, thereby influencing the cell cycle and proliferation. Collectively, our findings suggested that FAM83H‐AS1 participated in the progression of glioma and might act as a potential therapeutic target and prognosis biomarker for human glioma. 相似文献
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Effects of genome architecture and epigenetic factors on susceptibility of promoter CpG islands to aberrant DNA methylation induction 总被引：1，自引：0，他引：1
Aberrant DNA methylation is induced at specific promoter CpG islands (CGIs) in contrast with mutations. The specificity is influenced by genome architecture and epigenetic factors, but their relationship is still unknown. In this study, we isolated promoter CGIs susceptible and resistant to aberrant methylation induction during prostate and breast carcinogenesis. The effect of genome architecture was more evident for promoter CGIs susceptible in both of the two tissues than for promoter CGIs susceptible only in one tissue. Multivariate analysis of promoter CGIs with tissue-nonspecific susceptibility showed that genome architecture, namely a remote location from SINE (OR = 5.98; 95% CI = 2.33-15.34) and from LINE (OR = 2.08; 95% CI = 1.03-4.21), was associated with increased susceptibility, independent of epigenetic factors such as the presence of RNA polymerase II (OR = 0.09; 95% CI = 0.02-0.48) and H3K27me3 (OR = 3.28; 95% CI = 1.17-9.21). These results showed that methylation susceptibility of promoter CGIs is determined both by genome architecture and epigenetic factors, independently. 相似文献
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Hua‐Mao Wu Dong‐Jiang Xie Zuo‐Shun Tang Dong‐Qiao Shi Wei‐Cai Yang 《Plant biotechnology journal》2020,18(8):1778-1795