Magnesium (Mg 2+ ) is abundant in plant cells and plays a critical role in many physiological processes. A 10-member gene family AtMGT (also known as AtMRS2) was identified in Arabidopsis, which belongs to a eukaryote subset of the CorA superfamily, functioning as Mg 2+ transporters. Some family members (AtMGT1 and AtMGT10) function as high-affinity Mg 2+ transporter and could complement bacterial mutant or yeast mutant lacking Mg 2+ transport capability. Here we report an AtMGT family member, AtMGT9, that functions as a low-affinity Mg 2+ transporter, and is essential for pollen development. The functional complementation assay in Salmonella mutant strain MM281 showed that AtMGT9 is capable of mediating Mg 2+ uptake in the sub-millimolar range of Mg 2+ . The AtMGT9 gene was expressed most strongly in mature anthers and was also detectable in vascular tissues of the leaves, and in young roots. Disruption of AtMGT9 gene expression resulted in abortion of half of the mature pollen grains in heterozygous mutant +/mgt9, and no homozygous mutant plant was obtained in the progeny of selfed +/mgt9 plants. Transgenic plants expressing AtMGT9 in these heterozygous plants can recover the pollen phenotype to the wild type. In addition, At-MGT9 RNAi transgenic plants also showed similar abortive pollen phenotype to mutant +/mgt9. Together, our results demonstrate that AtMGT9 functions as a low-affinity Mg 2+ transporter that plays a crucial role in male gametophyte development and male fertility.
The plant elicitor peptides (Peps), a family of damage/danger-associated molecular patterns (DAMPs), are perceived by two receptors, PEPR1 and PEPR2, and contribute to plant defense against pathogen attack and abiotic stress. Here, we show that the Peps-PEPR signaling pathway functions in stomatal immunity by activating guard cell anion channels in The mutant plants lacking both and () displayed enhanced bacterial growth after being sprayed with pv () DC3000, but not after pathogen infiltration into leaves, implicating PEPR function in stomatal immunity. Indeed, synthetic Arabidopsis Peps (Peps) effectively induced stomatal closure in wild-type but not mutant leaves, suggesting that thePeps-PEPR signaling pathway triggers stomatal closure. Consistent with this finding, patch-clamp recording revealed Pep1-induced activation of anion channels in the guard cells of wild-type but not mutant plants. We further identified two guard cell-expressed anion channels, SLOW ANION CHANNEL1 (SLAC1) and its homolog SLAH3, as functionally overlapping components responsible for Pep1-induced stomatal closure. The double mutant, but not or single mutants, failed to respond to Pep1 in stomatal closure assays. Interestingly, disruption of (), an essential gene for abscisic acid-triggered stomatal closure, did not affect the Pep1-induced anion channel activity and stomatal response. Together, these results illustrate a DAMP-triggered signaling pathway that, unlike the flagellin22-FLAGELLIN-SENSITIVE2 pathway, triggers stomata immunity through an OST1-independent mechanism.
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