“…Efforts have focused on (1) transgenes targeting N uptake and transport, such as ammonium transporters [37], proton gradient-forming ATPases [38], or peptide/nitrate transporters [39]; (2) transgenes directly involved in primary N metabolism such as cytosolic glutamine synthetase (GS1;1 and GS1;2) [40,41,42], plastidic glutamine synthetase (GS2) [43], glutamate synthase (GOGAT) [44], glutamate dehydrogenase (GDH, [45] or primary and secondary N metabolism such as transaminases like asparagine synthetase (AS1) [46] and alanine aminotransferase (AlaAT) [12]; (3) transgenes involved in N recycling such as autophagy-related factor 8c (ATG8c, [47]); (4) regulatory factors such as the transcription factor Dof1 [48,49], microRNA826 [50], or microRNA444 [51]; (5) or N-responsive transgenes of unknown function such as the early nodulin 93-like gene [52]. Although there have not been any detailed metabolomics studies involving plants with genetically engineered NUE phenotypes, several studies have examined specific metabolite levels, some of these studies are listed in Table 2 [12,41,46,48,49,52,53,54]).…”