Balklava Zita, Rathnakumar Navin D, Vashist Shilpa, Schweinsberg Peter J, Grant Barth D
School of Life and Health Sciences, Aston University, Birmingham, B4 7ET, United Kingdom
School of Life and Health Sciences, Aston University, Birmingham, B4 7ET, United Kingdom.
Genetics. 2016 Sep;204(1):153-62. doi: 10.1534/genetics.116.188532. Epub 2016 Jul 22.
Inorganic phosphate is an essential mineral for both prokaryotic and eukaryotic cell metabolism and structure. Its uptake into the cell is mediated by membrane-bound transporters and coupled to Na(+) transport. Mammalian sodium-dependent Pi cotransporters have been grouped into three families NaPi-I, NaPi-II, and NaPi-III. Despite being discovered more than two decades ago, very little is known about requirements for NaPi-III transporters in vivo, in the context of intact animal models. Here we find that impaired function of the Caenorhabditis elegans NaPi-III transporter, pitr-1, results in decreased brood size and dramatically increased expression of vitellogenin by the worm intestine. Unexpectedly, we found that the effects of pitr-1 mutation on vitellogenin expression in the intestine could only be rescued by expression of pitr-1 in the germline, and not by expression of pitr-1 in the intestine itself. Our results indicate the existence of a signal from the germline that regulates gene expression in the intestine, perhaps linking nutrient export from the intestine to production of gametes by the germline.
无机磷酸盐是原核细胞和真核细胞新陈代谢及结构所必需的矿物质。它进入细胞是由膜结合转运蛋白介导的,并与钠(Na⁺)转运相偶联。哺乳动物钠依赖性磷酸盐共转运体已被分为三个家族:NaPi-I、NaPi-II和NaPi-III。尽管在二十多年前就已被发现,但在完整动物模型的背景下,对于体内NaPi-III转运体的需求却知之甚少。在此,我们发现秀丽隐杆线虫的NaPi-III转运体pitr-1功能受损会导致产卵量减少,并且线虫肠道中卵黄蛋白原的表达显著增加。出乎意料的是,我们发现pitr-1突变对肠道中卵黄蛋白原表达的影响只能通过在生殖系中表达pitr-1来挽救,而不能通过在肠道自身中表达pitr-1来挽救。我们的结果表明存在一种来自生殖系的信号,该信号调节肠道中的基因表达,也许将肠道中的营养物质输出与生殖系产生配子联系起来。