Background: In Arabidopsis, the aluminum (Al) exclusion mechanism is mainly facilitated by ALMT1-mediated malate exudation and MATE-mediated citrate releases from the root. Recently, we have demonstrated that coordinated functioning between the ALMT1-mediated exclusion mechanism, via exudation of malate from the root tip, and a NIP1;2-facilitated internal detoxification mechanism, via removal of Al from the root cell wall and subsequent root-to-shoot Al translocation, plays critical roles in achieving overall Al resistance. However, the genetic relationship between ALMT1 and NIP1;2 in these processes remained unclear.
Results: Through genetic and physiological analyses, we demonstrate that unlike ALMT1 and MATE, which function independently and additively, ALMT1 and NIP1;2 show an epistatic relationship in Al resistance in Arabidopsis. These results indicate that ALMT1 and NIP1;2 function in the same biochemical pathway, whereas ALMT1 and MATE in different biochemical pathways.
Conclusion: The establishment of the epistatic relationship and the coordinated functioning between the ALMT1 and NIP1;2-mediated exclusion and internal detoxification mechanisms are pivotal for achieving overall Al resistance in the non-accumulating Arabidopsis plant. We discuss and emphasize the indispensable roles of the root cell wall for the implementation of the Al exclusion mechanism and for the establishment of the epistatic relationship between the ALMT1-mediated exclusion mechanism and the NIP1;2-facilitated internal detoxification mechanism.

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On 11 Mar, 2020
On 11 Mar, 2020
On 09 Mar, 2020
On 02 Mar, 2020
On 01 Mar, 2020
On 01 Mar, 2020
On 01 Mar, 2020
Received 25 Feb, 2020
Invitations sent on 06 Feb, 2020
On 06 Feb, 2020
On 03 Feb, 2020
On 02 Feb, 2020
On 02 Feb, 2020
Posted 08 Oct, 2019
On 05 Jan, 2020
Received 23 Dec, 2019
On 09 Dec, 2019
On 29 Nov, 2019
Received 20 Nov, 2019
On 31 Oct, 2019
Invitations sent on 22 Oct, 2019
On 01 Oct, 2019
On 25 Sep, 2019
On 24 Sep, 2019
On 23 Sep, 2019
On 11 Mar, 2020
On 11 Mar, 2020
On 09 Mar, 2020
On 02 Mar, 2020
On 01 Mar, 2020
On 01 Mar, 2020
On 01 Mar, 2020
Received 25 Feb, 2020
Invitations sent on 06 Feb, 2020
On 06 Feb, 2020
On 03 Feb, 2020
On 02 Feb, 2020
On 02 Feb, 2020
Posted 08 Oct, 2019
On 05 Jan, 2020
Received 23 Dec, 2019
On 09 Dec, 2019
On 29 Nov, 2019
Received 20 Nov, 2019
On 31 Oct, 2019
Invitations sent on 22 Oct, 2019
On 01 Oct, 2019
On 25 Sep, 2019
On 24 Sep, 2019
On 23 Sep, 2019
Background: In Arabidopsis, the aluminum (Al) exclusion mechanism is mainly facilitated by ALMT1-mediated malate exudation and MATE-mediated citrate releases from the root. Recently, we have demonstrated that coordinated functioning between the ALMT1-mediated exclusion mechanism, via exudation of malate from the root tip, and a NIP1;2-facilitated internal detoxification mechanism, via removal of Al from the root cell wall and subsequent root-to-shoot Al translocation, plays critical roles in achieving overall Al resistance. However, the genetic relationship between ALMT1 and NIP1;2 in these processes remained unclear.
Results: Through genetic and physiological analyses, we demonstrate that unlike ALMT1 and MATE, which function independently and additively, ALMT1 and NIP1;2 show an epistatic relationship in Al resistance in Arabidopsis. These results indicate that ALMT1 and NIP1;2 function in the same biochemical pathway, whereas ALMT1 and MATE in different biochemical pathways.
Conclusion: The establishment of the epistatic relationship and the coordinated functioning between the ALMT1 and NIP1;2-mediated exclusion and internal detoxification mechanisms are pivotal for achieving overall Al resistance in the non-accumulating Arabidopsis plant. We discuss and emphasize the indispensable roles of the root cell wall for the implementation of the Al exclusion mechanism and for the establishment of the epistatic relationship between the ALMT1-mediated exclusion mechanism and the NIP1;2-facilitated internal detoxification mechanism.

Figure 1

Figure 2

Figure 3

Figure 4

Figure 5

Figure 6
This is a list of supplementary files associated with this preprint. Click to download.
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