Sequence upstream of the wheat (Triticum aestivum L.) ALMT1 gene and its relationship to aluminum resistance
Aluminum (Al) resistance in wheat relies on the Al-activated malate efflux from root' apices, which appears to be controlled by an Al-activated anion transporter encoded by the ALMT1 gene on chromosome 4DL. Genomic regions upstream and downstream of ALMT1 in 69 wheat lines were characterized to...
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Veröffentlicht in: | Plant and cell physiology 2006-10, Vol.47 (10), p.1343-1354 |
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Sprache: | eng |
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Zusammenfassung: | Aluminum (Al) resistance in wheat relies on the Al-activated malate efflux from root' apices, which appears to be controlled by an Al-activated anion transporter encoded by the ALMT1 gene on chromosome 4DL. Genomic regions upstream and downstream of ALMT1 in 69 wheat lines were characterized to identify patterns that might influence ALMT1 expression. The first 1,000 bp downstream of ALMT1 was conserved among the lines examined apart from the presence of a transposon-like sequence which did not correlate with Al resistance. In contrast, the first 1,000 bp upstream of the ALMT1 coding region was more variable and six different patterns could be discerned (types I-VI). Type I had the simplest structure, while the others had blocks of sequence that were duplicated or triplicated in different arrangements. A pattern emerged among the lines of non-Japanese origin such that the number of repeats in this upstream region was positively correlated with the levels of ALMT1 expression and Al resistance. In contrast, many of the Japanese lines exhibited a large variation in ALMT1 expression and Al resistance despite possessing the same type of upstream region. Although ALMT1 expression was also poorly correlated with Al-activated malate efflux in the Japanese lines, a strong correlation between malate efflux and Al resistance suggested that malate efflux was still the primary mechanism for Al resistance, and that additional genes are involved in the post-transcriptional regulation of ALMT1 function. |
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ISSN: | 0032-0781 1471-9053 |
DOI: | 10.1093/pcp/pcl002 |