McDowell Gary S, Lemire Joan M, Paré Jean-Francois, Cammarata Garrett, Lowery Laura Anne, Levin Michael
Biology Department, and Center for Regenerative and Developmental Biology, Tufts University, 200 Boston Avenue, Suite 4600, Medford, MA 02155-4243, USA.
Biology Department, Boston College, Chestnut Hill, MA, USA.
Integr Biol (Camb). 2016 Mar 14;8(3):267-86. doi: 10.1039/c5ib00281h.
Consistently-biased left-right (LR) patterning is required for the proper placement of organs including the heart and viscera. The LR axis is especially fascinating as an example of multi-scale pattern formation, since here chiral events at the subcellular level are integrated and amplified into asymmetric transcriptional cascades and ultimately into the anatomical patterning of the entire body. In contrast to the other two body axes, there is considerable controversy about the earliest mechanisms of embryonic laterality. Many molecular components of asymmetry have not been widely tested among phyla with diverse bodyplans, and it is unknown whether parallel (redundant) pathways may exist that could reverse abnormal asymmetry states at specific checkpoints in development. To address conservation of the early steps of LR patterning, we used the Xenopus laevis (frog) embryo to functionally test a number of protein targets known to direct asymmetry in plants, fruit fly, and rodent. Using the same reagents that randomize asymmetry in Arabidopsis, Drosophila, and mouse embryos, we show that manipulation of the microtubule and actin cytoskeleton immediately post-fertilization, but not later, results in laterality defects in Xenopus embryos. Moreover, we observed organ-specific randomization effects and a striking dissociation of organ situs from effects on the expression of left side control genes, which parallel data from Drosophila and mouse. Remarkably, some early manipulations that disrupt laterality of transcriptional asymmetry determinants can be subsequently "rescued" by the embryo, resulting in normal organ situs. These data reveal the existence of novel corrective mechanisms, demonstrate that asymmetric expression of Nodal is not a definitive marker of laterality, and suggest the existence of amplification pathways that connect early cytoskeletal processes to control of organ situs bypassing Nodal. Counter to alternative models of symmetry breaking during neurulation (via ciliary structures absent in many phyla), our data suggest a widely-conserved role for the cytoskeleton in regulating left-right axis formation immediately after fertilization of the egg. The novel mechanisms that rescue organ situs, even after incorrect expression of genes previously considered to be left-side master regulators, suggest LR patterning as a new context in which to explore multi-scale redundancy and integration of patterning from the subcellular structure to the entire bodyplan.
包括心脏和内脏在内的器官正确定位需要始终保持左右(LR)模式的偏向性。LR轴作为多尺度模式形成的一个例子特别引人入胜,因为在这里,亚细胞水平的手性事件被整合并放大为不对称转录级联反应,最终形成整个身体的解剖模式。与其他两个身体轴不同,关于胚胎左右性的最早机制存在相当大的争议。不对称的许多分子成分尚未在具有不同身体结构的门中广泛测试,并且尚不清楚是否可能存在平行(冗余)途径,这些途径可以在发育的特定检查点逆转异常的不对称状态。为了研究LR模式形成早期步骤的保守性,我们使用非洲爪蟾(青蛙)胚胎对一些已知在植物、果蝇和啮齿动物中指导不对称性的蛋白质靶点进行功能测试。使用与使拟南芥、果蝇和小鼠胚胎的不对称性随机化相同的试剂,我们发现受精后立即而非之后对微管和肌动蛋白细胞骨架进行操作会导致非洲爪蟾胚胎出现左右性缺陷。此外,我们观察到了器官特异性的随机化效应以及器官位置与左侧控制基因表达效应之间的显著分离,这与果蝇和小鼠的数据相似。值得注意的是,一些破坏转录不对称决定因素左右性的早期操作随后可以被胚胎“挽救”,从而导致正常的器官位置。这些数据揭示了新的纠正机制的存在,证明Nodal的不对称表达不是左右性的决定性标志,并表明存在将早期细胞骨架过程与绕过Nodal的器官位置控制相连接的放大途径。与神经胚形成过程中对称性打破的替代模型(通过许多门中不存在的纤毛结构)相反,我们的数据表明细胞骨架在卵子受精后立即调节左右轴形成中具有广泛保守的作用。即使在先前被认为是左侧主调节因子的基因表达错误之后仍能挽救器官位置的新机制,表明LR模式形成是一个新的背景,可用于探索从亚细胞结构到整个身体结构的多尺度冗余和模式整合。