Present address: MRC Human Genetics Unit, Western General Hospital, Crewe Road, Edinburgh, UK.
Evidence for a role in growth and salt resistance of a plasma membrane H+-ATPase in the root endodermis
Article first published online: 23 DEC 2001
The Plant Journal
Volume 27, Issue 3, pages 191–201, August 2001
How to Cite
Vitart, V., Baxter, I., Doerner, P. and Harper, J. F. (2001), Evidence for a role in growth and salt resistance of a plasma membrane H+-ATPase in the root endodermis. The Plant Journal, 27: 191–201. doi: 10.1046/j.1365-313x.2001.01081.x
- Issue published online: 23 DEC 2001
- Article first published online: 23 DEC 2001
- Received 3 April 2001; accepted 26 April 2001.
- salt stress;
The plasma membrane of plant cells is energized by an electrochemical gradient produced by P-type H+-ATPases (proton pumps). These pumps are encoded by at least 12 genes in Arabidopsis. Here we provide evidence that isoform AHA4 contributes to solute transport through the root endodermis. AHA4 is expressed most strongly in the root endodermis and flowers, as suggested by promoter-GUS reporter assays. A disruption of this pump (aha4–1) was identified as a T-DNA insertion in the middle of the gene (after VFP574). Truncated aha4–1 transcripts accumulate to approximately 50% of the level observed for AHA4 mRNA in wild-type plants. Plants homozygous for aha4–1 (–/–) show a subtle reduction in root and shoot growth compared with wild-type plants when grown under normal conditions. However, a mutant phenotype is very clear in plants grown under salt stress (e.g., 75 or 110 mm NaCl). In leaves of mutant plants subjected to Na stress, the ratio of Na to K increased 4–5-fold. Interestingly, the aha4–1 mutation appears to be semidominant and was only partially complemented by the introduction of additional wild-type copies of AHA4. These results are consistent with the hypothesis that aha4–1 may produce a dominant negative protein or RNA that partially disrupts the activity of other pumps or functions in the root endodermal tissue, thereby compromising the function of this cell layer in controlling ion homeostasis and nutrient transport.