Functional contribution of DCLKs in sea urchin development.
Functional contribution of DCLKs in sea urchin development.
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DOI：
10.1002/dvdy.316
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发表时间：
2021-08
期刊：
影响因子：
--
通讯作者：
Yajima M
中科院分区：
文献类型：
--
作者：
Xu D;Wavreil FDM;Waldron A;Yajima M
双皮质素样激酶1和2 （DCLKs）是蛋白丝氨酸/苏氨酸激酶，在神经元发育中起重要作用。最近，它们也被报道调节可塑性，如干细胞和癌细胞的细胞增殖和分化，但它们在这种生物学背景下的功能细节仍不清楚。为了揭示DCLKs在可塑性调控中的作用，我们以高度调控发育的海胆胚胎为实验模型。我们发现DCLKs的转录本和蛋白质在胚胎发生早期均匀存在，并在原胚期后的间充质细胞中有所富集。DCLKs基因敲低会在第2天引起一般发育迟缓和缺陷。此外，胚胎/幼虫的损伤诱导DCLKs在损伤最严重的外胚层异位表达。在肿瘤易发或抑制条件下，损伤后DCLKs的表达分别上调或下调。在这两种情况下，胚胎都表现出严重的发育缺陷。综上所述，dclk的短暂上调似乎与正常和异常发育期间的损伤反应有关，并可能以依赖于环境的方式导致不同的表型。
Doublecortin-like kinase1 and 2 (DCLKs) are protein Ser/Thr kinases important for neuronal development. More recently, they are also reported to regulate plasticity such as cell proliferation and differentiation of stem cells and cancer cells, but the details of their functions in this biological context are still unclear. With an attempt to reveal the functions of DCLKs in plasticity regulation, we here used the sea urchin embryo that undergoes highly regulative development as an experimental model. We found that both the transcripts and the proteins of DCLKs are uniformly present during early embryogenesis and with some enrichment in mesenchymal cells after gastrula stage. Knockdown of DCLKs induced general developmental delay and defects at day 2. Further, the damage on the embryo/larva induced ectopic expression of DCLKs in the ectoderm where the damage was most severe. Under a tumor-prone or -suppressive condition, DCLKs expression was upregulated or downregulated, respectively, after damage. In both cases, the embryos showed severe developmental defects. Taken together, a transient upregulation of DCLKs appears to be involved in a damage response both during normal and abnormal development, and which could result in different phenotypes in a context dependent manner.
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