Thompson Kenneth W, Joshi Pradeep, Dymond Jessica S, Gorrepati Lakshmi, Smith Harold E, Krause Michael W, Eisenmann David M
Department of Biological Sciences, University of Maryland Baltimore County, 1000 Hilltop Circle, Baltimore, MD 21250, USA.
National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 5 Center Drive, Bethesda, MD 20892, USA.
Dev Biol. 2016 Apr 15;412(2):191-207. doi: 10.1016/j.ydbio.2016.03.002. Epub 2016 Mar 4.
The development of the single cell layer skin or hypodermis of Caenorhabditis elegans is an excellent model for understanding cell fate specification and differentiation. Early in C. elegans embryogenesis, six rows of hypodermal cells adopt dorsal, lateral or ventral fates that go on to display distinct behaviors during larval life. Several transcription factors are known that function in specifying these major hypodermal cell fates, but our knowledge of the specification of these cell types is sparse, particularly in the case of the ventral hypodermal cells, which become Vulval Precursor Cells and form the vulval opening in response to extracellular signals. Previously, the gene pvl-4 was identified in a screen for mutants with defects in vulval development. We found by whole genome sequencing that pvl-4 is the Paired-box gene pax-3, which encodes the sole PAX-3 transcription factor homolog in C. elegans. pax-3 mutants show embryonic and larval lethality, and body morphology abnormalities indicative of hypodermal cell defects. We report that pax-3 is expressed in ventral P cells and their descendants during embryogenesis and early larval stages, and that in pax-3 reduction-of-function animals the ventral P cells undergo a cell fate transformation and express several markers of the lateral seam cell fate. Furthermore, forced expression of pax-3 in the lateral hypodermal cells causes them to lose expression of seam cell markers. We propose that pax-3 functions in the ventral hypodermal cells to prevent these cells from adopting the lateral seam cell fate. pax-3 represents the first gene required for specification solely of the ventral hypodermal fate in C. elegans providing insights into cell type diversification.
秀丽隐杆线虫单细胞层皮肤或皮下组织的发育是理解细胞命运特化和分化的优秀模型。在秀丽隐杆线虫胚胎发育早期,六排皮下细胞采用背侧、外侧或腹侧命运,这些细胞在幼虫期会表现出不同的行为。已知有几种转录因子在确定这些主要的皮下细胞命运中发挥作用,但我们对这些细胞类型特化的了解还很匮乏,尤其是腹侧皮下细胞的情况,这些细胞会变成外阴前体细胞,并根据细胞外信号形成外阴开口。此前,在一项针对外阴发育缺陷突变体的筛选中鉴定出了基因pvl-4。我们通过全基因组测序发现pvl-4是配对盒基因pax-3,它编码秀丽隐杆线虫中唯一的PAX-3转录因子同源物。pax-3突变体表现出胚胎和幼虫致死性,以及表明皮下细胞缺陷的身体形态异常。我们报告称,pax-3在胚胎发育和幼虫早期阶段在腹侧P细胞及其后代中表达,并且在pax-3功能降低的动物中,腹侧P细胞会经历细胞命运转变,并表达几种外侧缝线细胞命运的标记物。此外,在外侧皮下细胞中强制表达pax-3会导致它们失去缝线细胞标记物的表达。我们提出,pax-3在腹侧皮下细胞中发挥作用,以防止这些细胞采用外侧缝线细胞命运。pax-3代表了秀丽隐杆线虫中仅确定腹侧皮下命运所需的第一个基因,为细胞类型多样化提供了见解。