DIFFERENTIAL REGULATION OF SUGAR-SENSITIVE SUCROSE SYNTHASES BY HYPOXIA AND ANOXIA INDICATE COMPLEMENTARY TRANSCRIPTIONAL AND POSTTRANSCRIPTIONAL RESPONSES

The goal of this research was to resolve the hypoxic and anoxic respon ses of maize (Zea mays) sucrose (Suc) synthases known to differ in the ir sugar regulation. The two maize Suc synthase genes, Sus1 and Sh1, b oth respond to sugar and O-2, and recent work suggests commonalities b etween these signaling systems. Maize seedlings (NK508 hybrid, W22 inb red, and an isogenic shf-null mutant) were exposed to anoxic, hypoxic, and aerobic conditions (0, 3, and 21% O-2, respectively), when primar y roots had reached approximately 5 cm. One-centimeter tips were excis ed for analysis during the 48-h treatments. At the mRNA level, Sus1 wa s rapidly up-regulated by hypoxia (approximately 5-fold in 6 h), where as anoxia had less effect. in contrast, Sh1 mRNA abundance increased s trongly under anoxia (approximately 5-fold in 24 h) and was much less affected by hypoxia. At the enzyme level, total Suc synthase activity rose rapidly under hypoxia but showed little significant change during anoxia. The contributions of SUS1 and SH1 activities to these respons es were dissected over time by comparing the sh1-null mutant with the isogenic wild type (Sus+, Sh1+). Sh1-dependent activity contributed mo st markedly to a rapid protein-level response consistently observed in the first 3 h, and, subsequently, to a long-term change mediated at t he level of mRNA accumulation at 48 h. A complementary midterm rise in SUS1 activity varied in duration with genetic background. These data highlight the involvement of distinctly different genes and probable s ignal mechanisms under hypoxia and anoxia, and together with earlier w ork, show parallel induction of ''feast and famine'' Suc synthase gene s by hypoxia and anoxia, respectively. in addition, complementary mode s of transcriptional and posttranscriptional regulation are implicated by these data, and provide a mechanism for sequential contributions f rom the Sus1 and Sh1 genes during progressive onset of naturally occur ring low-O-2 events.