Department of Microbiology, University of Georgia, Athens, Georgia, USA.
Department of Chemistry, University of Tennessee, Knoxville, Tennessee, USA.
J Biol Chem. 2021 Jan-Jun;296:100651. doi: 10.1016/j.jbc.2021.100651. Epub 2021 Apr 9.
The Rid protein family (PF14588, IPR006175) is divided into nine subfamilies, of which only the RidA subfamily has been characterized biochemically. RutC, the founding member of one subfamily, is encoded in the pyrimidine utilization (rut) operon that encodes a pathway that allows Escherichia coli to use uracil as a sole nitrogen source. Results reported herein demonstrate that RutC has 3-aminoacrylate deaminase activity and facilitates one of the reactions previously presumed to occur spontaneously in vivo. RutC was active with several enamine-imine substrates, showing similarities and differences in substrate specificity with the canonical member of the Rid superfamily, Salmonella enterica RidA. Under standard laboratory conditions, a Rut pathway lacking RutC generates sufficient nitrogen from uracil for growth of E. coli. These results support a revised model of the Rut pathway and provide evidence that Rid proteins may modulate metabolic fitness, rather than catalyzing essential functions.
Rid 蛋白家族（PF14588，IPR006175）分为九个亚家族，其中只有 RidA 亚家族在生化上得到了表征。RutC 是一个亚家族的创始成员，它编码在嘧啶利用（rut）操纵子中，该操纵子编码了一条途径，使大肠杆菌能够将尿嘧啶作为唯一的氮源。本文报道的结果表明，RutC 具有 3-氨基丙烯酸脱氨酶活性，并促进了先前在体内被认为自发发生的反应之一。RutC 对几种烯胺-亚胺底物具有活性，与经典的 Rid 超家族成员沙门氏菌 RidA 的底物特异性有相似之处和不同之处。在标准实验室条件下，缺乏 RutC 的 Rut 途径从尿嘧啶中产生足够的氮以供大肠杆菌生长。这些结果支持了 Rut 途径的修正模型，并提供了证据表明 Rid 蛋白可能调节代谢适应性，而不是催化必需功能。
