The Glycine- and Proline-Rich Protein AtGPRP3 Negatively Regulates Plant Growth in Arabidopsis

Glycine- and proline-rich proteins (GPRPs) comprise a small conserved family that is widely distributed in the plant kingdom. GPRPs are relatively short peptides (<200 amino acids) that contain three typical domains, including an N-terminal XYPP-repeat domain, a middle hydrophobic domain rich in alanine, and a C-terminal HGK-repeat domain. These proteins have been proposed to play fundamental roles in plant growth and environmental adaptation, but their functions remain unknown. In this study, we selected an Arabidopsis GPRP (AtGPRP3) to profile the physiological role of GPRPs. Transcripts of AtGPRP3 could be detected in the whole Arabidopsis plant, but greater amounts were found in the rosette, followed by the cauline. The AtGPRP3::GFP fusion protein was mainly localized in the nucleus. The overexpression and knockout of AtGPRP3, respectively, retarded and accelerated the growth of Arabidopsis seedlings, while the increase in the growth rate of atgprp3 plants was offset by the complementary expression of AtGPRP3. CAT2 and CAT3, but not CAT1, interacted with AtGPRP3 in the nuclei of Arabidopsis protoplasts. The knockout of CAT2 by CRISPR-Cas9 retarded the growth of the Arabidopsis seedlings. Together, our data suggest that AtGPRP3 negatively regulates plant growth, potentially through CAT2 and CAT3.

An exclusion mechanism is epistatic to an internal detoxification mechanism in aluminum resistance in Arabidopsis

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 Al 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. These results indicate that ALMT1 and NIP1;2 function in the same biochemical pathway, whereas ALMT1 and MATE in different ones.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 an epistatic relationship between the ALMT1-mediated exclusion mechanism and the NIP1;2-facilitated internal detoxification mechanism.

An exclusion mechanism is epistatic to an internal detoxification mechanism in aluminum resistance in Arabidopsis

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 Al 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. These results indicate that ALMT1 and NIP1;2 function in the same biochemical pathway, whereas ALMT1 and MATE in different ones.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 an epistatic relationship between the ALMT1-mediated exclusion mechanism and the NIP1;2-facilitated internal detoxification mechanism.

An exclusion mechanism is epistatic to an internal detoxification mechanism in aluminum resistance in Arabidopsis

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 Al 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. These results indicate that ALMT1 and NIP1;2 function in the same biochemical pathway, whereas ALMT1 and MATE in different ones. 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 an epistatic relationship between the ALMT1-mediated exclusion mechanism and the NIP1;2-facilitated internal detoxification mechanism.