jaw-1D: a gain-of-function mutation responsive to paramutation-like induction of epigenetic silencing.

jaw-1D: a gain-of-function mutation responsive to paramutation-like induction of epigenetic silencing.
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jaw-1D:一种功能获得性突变,对表观遗传沉默的副突变诱导有反应

DOI:
10.1093/jxb/ery365
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发表时间:
2019-01-07
影响因子:
6.9
通讯作者:
Dong A
Dong A
中科院分区:
生物学1区
文献类型:
--
作者:
Jiang W;Li Z;Yao X;Zheng B;Shen WH;Dong A

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拟南芥功能获得性T-DNA插入突变体jaw-1D具有一种意想不到的副突变现象,该现象是由具有多拷贝串联T-DNA重复序列的转基因SALK突变系引起的。拟南芥功能获得性T-DNA插入突变体jaw-1D产生miR 319 A,miR 319 A是一种抑制编码CIN样TEOSINTE BRANCHED 1/Cycloidea/PROLIFERATING CELL FACTORS(TCPs)的基因的microRNA,TCPs是在叶形态发生中起关键作用的转录因子家族。在这项研究中,我们表明,颌骨-1D是副突变样表观遗传沉默。jaw-1D与polycomb基因突变体卷曲叶-29(clf-29)的遗传杂交导致jaw-1D突变体植物表型的衰减。这种诱导突变,jaw-1D*,与miR 319 A的下调相关,可独立于clf-29遗传,并显示副突变样非孟德尔遗传。miR 319 A在jaw-1D* 中的下调与组蛋白H3赖氨酸9二甲基化和位于jaw-1D基因座的激活标记T-DNA内的CaMV 35 S增强子处的DNA甲基化水平升高有关。检查21个独立的T-DNA插入突变株系发现,11个可以减弱的jaw-1D突变表型以类似的方式由clf-29诱导的副突变。这些副突变株系的共同特征是T-DNA插入以多拷贝串联重复序列的形式存在,并含有高水平的CG和CHG甲基化。我们的研究结果提供了重要的见解paramutation样表观遗传沉默,并警告对使用的jaw-1D的遗传相互作用的研究。
An Arabidopsis gain-of-function T-DNA insertion mutant, jaw-1D, has an unexpected paramutation phenomenon caused by transgenic SALK mutant lines with multi-copy tandem T-DNA repeats. The Arabidopsis thaliana gain-of-function T-DNA insertion mutant jaw-1D produces miR319A, a microRNA that represses genes encoding CIN-like TEOSINTE BRANCHED1/CYCLOIDEA/PROLIFERATING CELL FACTORs (TCPs), a family of transcription factors that play key roles in leaf morphogenesis. In this study, we show that jaw-1D is responsive to paramutation-like epigenetic silencing. A genetic cross of jaw-1D with the polycomb gene mutant curly leaf-29 (clf-29) leads to attenuation of the jaw-1D mutant plant phenotype. This induced mutation, jaw-1D*, was associated with down-regulation of miR319A, was heritable independently from clf-29, and displayed paramutation-like non-Mendelian inheritance. Down-regulation of miR319A in jaw-1D* was linked to elevated levels of histone H3 lysine 9 dimethylation and DNA methylation at the CaMV35S enhancer located within the activation-tagging T-DNA of the jaw-1D locus. Examination of 21 independent T-DNA insertion mutant lines revealed that 11 could attenuate the jaw-1D mutant phenotype in a similar way to the paramutation induced by clf-29. These paramutagenic mutant lines shared the common feature that their T-DNA insertion was present as multi-copy tandem repeats and contained high levels of CG and CHG methylation. Our results provide important insights into paramutation-like epigenetic silencing, and caution against the use of jaw-1D in genetic interaction studies.
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