Submitted to: Plant Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/28/1996
Publication Date: N/A
Citation: N/A Interpretive Summary: 1) Rationale: The goal here was to isolate and determine the full DNA sequence (genetic code) of the gene encoding an enzyme that appears to be responsible for the formation of 'air sacs' in maize roots during flooding, and to determine if gene expression is correlated with air sac formation. 2) Accomplishments: The DNAs were isolated and the sequence obtained and analyzed. Expression of the gene was found to be correlated with air sac formation, however it is also expressed at other times. 3) Significance: The understanding of the role of this gene, in terms of its protein synthesis in response to flooding and developmental changes it may be responsible for, may allow for effective methods to produce crop plants that are tolerant to flooding.
Technical Abstract: Flooded plants undergo structural modifications which are usually manifested in the formation of intercellular air spaces (aerenchyma). Aerenchyma, which are promoted by endogenous ethylene, result from cell wall degradation and cell lysis in cortical tissues. Despite their adaptive significance, the molecular mechanisms behind aerenchyma formation remain unknown. We recently isolated a flooding-induced maize (Zea mays L.) gene (wusl1005(gfu); abbreviated as 1005) encoding a homolog of xyloglucan endo-transglycosylase (XET), a putative cell wall loosening enzyme active during germination, expansion, and fruit softening. Thus, XET may also be involved in cell wall metabolism during flooding-induced aerenchyma formation. Under flooding, 1005 mRNA accumulated in root and mesocotyl locations that subsequently underwent aerenchyma formation, and reached maximum levels within 12 h of treatment. Visible cell lysis was observed in the same locations by 48 h of treatment. Treatment with the ethylene synthesis inhibitor (aminooxy)acetic acid (AOA) almost completely inhibited 1005 mRNA accumulation under flooding in both organs, suggesting that 1005 induction by flooding is responsive to ethylene accumulation. AOA treatment had little effect on the accumulation of mRNA encoded by adh1, another flooding-responsive gene, indicating that it did not cause a general suppression of flooding-responsive genes. Additionally, 1005 was induced in both organs by ethylene treatment under fully aerobic conditions, providing further evidence for its responsiveness to ethylene. In contrast to flooding, however, AOA treatment under anoxia did not affect 1005 mRNA accumulation, suggesting that 1005 is induced via different mechanisms under flooding (hypoxia) and anoxia.