Bui Linh T, Ragsdale Erik J
Department of Biology, Indiana University, Bloomington, IN.
Mol Biol Evol. 2019 Nov 1;36(11):2387-2399. doi: 10.1093/molbev/msz171.
The ability to translate a single genome into multiple phenotypes, or developmental plasticity, defines how phenotype derives from more than just genes. However, to study the evolutionary targets of plasticity and their evolutionary fates, we need to understand how genetic regulators of plasticity control downstream gene expression. Here, we have identified a transcriptional response specific to polyphenism (i.e., discrete plasticity) in the nematode Pristionchus pacificus. This species produces alternative resource-use morphs-microbivorous and predatory forms, differing in the form of their teeth, a morphological novelty-as influenced by resource availability. Transcriptional profiles common to multiple polyphenism-controlling genes in P. pacificus reveal a suite of environmentally sensitive loci, or ultimate target genes, that make up an induced developmental response. Additionally, in vitro assays show that one polyphenism regulator, the nuclear receptor NHR-40, physically binds to promoters with putative HNF4α (the nuclear receptor class including NHR-40) binding sites, suggesting this receptor may directly regulate genes that describe alternative morphs. Among differentially expressed genes were morph-limited genes, highlighting factors with putative "on-off" function in plasticity regulation. Further, predatory morph-biased genes included candidates-namely, all four P. pacificus homologs of Hsp70, which have HNF4α motifs-whose natural variation in expression matches phenotypic differences among P. pacificus wild isolates. In summary, our study links polyphenism regulatory loci to the transcription producing alternative forms of a morphological novelty. Consequently, our findings establish a platform for determining how specific regulators of morph-biased genes may influence selection on plastic phenotypes.
将单个基因组转化为多种表型的能力，即发育可塑性，决定了表型不仅仅源于基因。然而，为了研究可塑性的进化靶点及其进化命运，我们需要了解可塑性的遗传调控因子如何控制下游基因表达。在此，我们在太平洋普氏线虫中鉴定出了一种对多型现象（即离散可塑性）特异的转录反应。该物种会产生不同的资源利用形态——微生物食性和捕食性形态，其牙齿形态不同，这是一种形态学上的新奇特征，受资源可用性影响。太平洋普氏线虫中多个控制多型现象的基因共有的转录谱揭示了一组对环境敏感的位点，即最终靶基因，它们构成了一种诱导性发育反应。此外，体外实验表明，一种多型现象调控因子，核受体NHR - 40，与具有假定HNF4α（包括NHR - 40的核受体类别）结合位点的启动子发生物理结合，这表明该受体可能直接调控描述不同形态的基因。在差异表达基因中存在形态受限基因，突出了在可塑性调控中具有假定“开 - 关”功能的因子。此外，捕食性形态偏向基因包括一些候选基因——即Hsp70的所有四个太平洋普氏线虫同源物，它们具有HNF4α基序——其表达的自然变异与太平洋普氏线虫野生分离株之间的表型差异相匹配。总之，我们的研究将多型现象调控位点与产生形态学新奇特征替代形式的转录联系起来。因此，我们的发现建立了一个平台，用于确定形态偏向基因的特定调控因子如何影响对可塑性表型的选择。
