MicroRNAs prevent precocious gene expression and enable pattern formation during plant embryogenesis
MicroRNAs prevent precocious gene expression and enable pattern formation during plant embryogenesis
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DOI：
10.1101/gad.1986710
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发表时间：
2010-12-01
影响因子：
10.5
通讯作者：
Bartel, David P.
中科院分区：
文献类型：
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作者：
Nodine, Michael D.;Bartel, David P.
拟南芥胚胎缺乏microRNA （miRNA）生物发生所必需的DICER-LIKE1 (DCL1)，会在发育早期停滞。为了评估胚胎mirna的功能，我们确定了DCL1缺失的发育和分子后果。我们发现早在8细胞期，DCL1是细胞分化事件所必需的，随后是垂体和亚原胚层细胞的正常分裂所必需的。在早期球形（类似于32细胞）阶段，dcl1缺失突变胚胎过表达类似于50个miRNA靶点。在dcl1八细胞胚胎中，两个上调最多的靶标是miR156，它们编码SPL10和SPL11转录因子。SPL10和SPL11在dcl1胚胎中被抑制了150倍，并且是dcl1早期模式缺陷所必需的。此外，早在八细胞期，mir156介导的合子SPL转录物的抑制阻止了胚胎成熟期正常诱导的基因转录物的过早积累。因此，植物胚胎mirna的第一个可感知的分子功能与脊椎动物的相反；在脊椎动物中，mirna加强了第一次发育转变，而在植物中，它们通过抑制后来起作用的mrna来阻止发育转变。我们认为，通过阻止促分化转录因子的过早表达，mirna可以实现正确的胚胎模式。
Arabidopsis embryos lacking DICER-LIKE1 (DCL1), which is required for microRNA (miRNA) biogenesis, arrest early in development. To assess the functions of embryonic miRNAs, we determined the developmental and molecular consequences of DCL1 loss. We found that DCL1 is required for cell differentiation events as early as the eight-cell stage and soon thereafter for proper division of the hypophysis and subprotoderm cells. By the early globular (similar to 32-cell) stage, dcl1-null mutant embryos overexpress similar to 50 miRNA targets. In dcl1 eight-cell embryos, the two most up-regulated targets are those of miR156 and encode SPL10 and SPL11 transcription factors. SPL10 and SPL11 are derepressed >150-fold in dcl1 embryos and are redundantly required for the dcl1 early patterning defects. Moreover, as early as the eight-cell stage, miR156-mediated repression of zygotic SPL transcripts prevents premature accumulation of transcripts from genes normally induced during the embryonic maturation phase. Thus, the first perceptible molecular function of plant embryonic miRNAs is the opposite of that in vertebrates; in vertebrates, miRNAs sharpen the first developmental transition, whereas in plants, they forestall developmental transitions by repressing mRNAs that act later. We propose that, by preventing precocious expression of differentiation-promoting transcription factors, miRNAs enable proper embryonic patterning.