ADAR proteins alter gene expression both by catalyzing adenosine (A) to inosine (I) RNA editing and binding to regulatory elements in target RNAs. Loss of ADARs affects neuronal function in all animals studied to date. Caenorhabditis elegans lacking ADARs exhibit reduced chemotaxis, but the targets responsible for this phenotype remain unknown. To identify critical neural ADAR targets in C. elegans, we performed an unbiased assessment of the effects of ADR-2, the only A-to-I editing enzyme in C. elegans, on the neural transcriptome. Development and implementation of publicly available software, SAILOR, identified 7,361 A-to-I editing events across the neural transcriptome. Intersecting the neural editome with adr-2 associated gene expression changes, revealed an edited mRNA, clec-41, whose neural expression is dependent on deamination. Restoring clec-41 expression in adr-2 deficient neural cells rescued the chemotaxis defect, providing the first evidence that neuronal phenotypes of ADAR mutants can be caused by altered gene expression.

ADAR蛋白通过催化腺苷（A）到肌苷（I）RNA编辑以及与靶RNA中的调控元件的结合来改变基因表达。迄今为止，ADAR的丧失会影响所有动物的神经元功能。缺乏ADAR的秀丽隐杆线虫显示趋化性降低，但导致该表型的靶标仍未知。为了找出关键的神经ADAR目标线虫，我们进行的ADR-2，在只有A到I编辑酶的影响客观公正的评估线虫，对神经转录。公开可用的软件SAILOR的开发和实现，在整个神经转录组中识别出7,361个A-to-I编辑事件。将神经编辑组与adr-2相交相关基因表达的变化，揭示了一个编辑过的mRNA，clec-41，其神经表达依赖于脱氨基作用。恢复adr-2缺陷神经细胞中clec-41的表达可以挽救趋化性缺陷，这提供了第一个证据表明ADAR突变体的神经元表型可能是由基因表达的改变引起的。