AtFTCD-L, a trans-Golgi network localized protein, modulates root growth of Arabidopsis in high-concentration agar culture medium.

MAIN CONCLUSION: AtFTCD-L protein is localized on the TGN vesicles in Arabidopsis root cap cells. AtFTCD-L mutation resulted in slow root growth of Arabidopsis in high-concentration agar culture medium. Arabidopsis formiminotransferase cyclodeaminase-like protein (AtFTCD-L) in Arabidopsis is homologous to the formiminotransferase cyclodeaminase (FTCD) protein in animal cells. However, the localization and function of AtFTCD-L remain unknown in Arabidopsis. In this study, we generated and analyzed a deletion mutant of AtFTCD-L with a T-DNA insertion. We found that the growth of Arabidopsis roots with the T-DNA insertion mutation in AtFTCD-L was slower than that of wild-type roots when grown in high-concentration 1/2 MS agar culture medium. AtFTCD-L-GFP could restore the ftcd-l mutant phenotype. In addition, the AtFTCD-L protein was localized on the trans-Golgi network (TGN) vesicles in Arabidopsis root cap cells. Fluorescence recovery after photobleaching (FRAP) experiment using Arabidopsis pollen-specific receptor-like kinase-GFP (AtPRK1-GFP) stably transformed plants showed that the deficiency of AtFTCD-L protein in Arabidopsis led to slower secretion in the root cap peripheral cells. The AtFTCD-L protein deficiency also resulted in a significantly reduced monosaccharides content in the culture medium. Based on the above results, we speculate that the AtFTCD-L protein may be involved in sorting and/or transportation of TGN vesicles in root cap peripheral cells, thereby regulating the extracellular secretion of mucilage components in the root cap.

Mechanisms used by DNA MMR system to cope with Cadmium-induced DNA damage in plants.

Cadmium (Cd) is found widely in soil and is severely toxic for plants, causing oxidative damage in plant cells because of its heavy metal characteristics. The DNA damage response (DDR) is triggered in plants to cope with the Cd stress. The DNA mismatch repair (MMR) system known for its mismatch repair function determines DDR, as mispairs are easily generated by a translesional synthesis under Cd-induced genomic instability. Cd-induced mismatches are recognized by three heterodimeric complexes including MutSα (MSH2/MSH6), MutSß (MSH2/MSH3), and MutSγ (MSH2/MSH7). MutLα (MLH1/PMS1), PCNA/RFC, EXO1, DNA polymerase δ and DNA ligase participate in mismatch repair in turn. Meanwhile, ATR is preferentially activated by MSH2 to trigger DDR including the regulation of the cell cycle, endoreduplication, cell death, and recruitment of other DNA repair, which enhances plant tolerance to Cd. However, plants with deficient MutS will bypass MMR-mediated DDR and release the multiple-effect MLH1 from requisition of the MMR system, which leads to weak tolerance to Cd in plants. In this review, we systematically illustrate how the plant DNA MMR system works in a Cd-induced DDR, and how MMR genes regulate plant tolerance to Cd. Additionally, we also reviewed multiple epigenetic regulation systems acting on MMR genes under stress.

Corrigendum: Arabidopsis PCaP2 Functions as a Linker Between ABA and SA Signals in Plant Water Deficit Tolerance.

[This corrects the article DOI: 10.3389/fpls.2018.00578.].

Arabidopsis PCaP2 Functions as a Linker Between ABA and SA Signals in Plant Water Deficit Tolerance.

Water stress has a major influence on plant growth, development, and productivity. However, the cross-talk networks involved in drought tolerance are not well understood. Arabidopsis PCaP2 is a plasma membrane-associated Ca2+-binding protein. In this study, we employ qRT-PCR and ß-glucuronidase (GUS) histochemical staining to demonstrate that PCaP2 expression was strongly induced in roots, cotyledons, true leaves, lateral roots, and whole plants under water deficit conditions. Compared with the wild type (WT) plants, PCaP2-overexpressing (PCaP2-OE) plants displayed enhanced water deficit tolerance in terms of seed germination, seedling growth, and plant survival status. On the contrary, PCaP2 mutation and reduction via PCaP2-RNAi rendered plants more sensitive to water deficit. Furthermore, PCaP2-RNAi and pcap2 seedlings showed shorter root hairs and lower relative water content compared to WT under normal conditions and these phenotypes were exacerbated under water deficit. Additionally, the expression of PCaP2 was strongly induced by exogenous abscisic acid (ABA) and salicylic acid (SA) treatments. PCaP2-OE plants showed insensitive to exogenous ABA and SA treatments, in contrast to the susceptible phenotypes of pcap2 and PCaP2-RNAi. It is well-known that SNF1-related kinase 2s (SnRK2s) and pathogenesis-related (PRs) are major factors that influence plant drought tolerance by ABA- and SA-mediated pathways, respectively. Interestingly, PCaP2 positively regulated the expression of drought-inducible genes (RD29A, KIN1, and KIN2), ABA-mediated drought responsive genes (SnRK2.2, -2.3, -2.6, ABF1, -2, -3, -4), and SA-mediated drought responsive genes (PR1, -2, -5) under water deficit, ABA, or SA treatments. Taken together, our results showed that PCaP2 plays an important and positive role in Arabidopsis water deficit tolerance by involving in response to both ABA and SA signals and regulating root hair growth. This study provides novel insights into the underlying cross-talk mechanisms of plants in response to water deficit stress.

Arabidopsis PCaP2 Plays an Important Role in Chilling Tolerance and ABA Response by Activating CBF- and SnRK2-Mediated Transcriptional Regulatory Network.

Chilling stress affects plant growth and productivity. However, the multi-underlying mechanisms of chilling tolerance are not well understood. Arabidopsis PCaP2 is involved in regulating the dynamic of microtubules (MTs) and F-actin and Ca2+-binding ability. Here, the results showed that the PCaP2 expression was highly induced in roots, cotyledons, true leaves, lateral roots and flowers under cold stress. Compared with the wild type, PCaP2-overexpressing plants displayed the enhanced tolerance, whereas its RNAi and mutant were more sensitive in seed germination, seedling and reproductive growth under chilling stress in Arabidopsis. In addition, PCaP2 was also a positive regulator of ABA signaling pathway by analyzing the expression of PCaP2 and the phenotypes of PCaP2-overexpressing, mutant and RNAi plants under ABA treatment. Interestingly, disruption of PCaP2 inhibited the expression of CBF1, -3 and CBF-target COR genes, while increased the CBF2 expression in response to cold or ABA. Moreover, we found that SnRK2s were involved in cold stress and PCaP2 mutants down-regulated the transcription level of SnRK2.2, -2.3 and SnRK2-mediated downstream genes including ABF2, RD29A, KIN1, KIN2, but up-regulated SnRK2.6, ABF1, -3, -4 in ABA and cold treatments. It is well-accepted that PCaP2 as a Ca2+-binding protein triggers the gene expression to enhance plant chilling tolerance. Our further studies showed that MT destabilizing activity of PCaP2, but not F-actin-severing function, may be involved in chilling stress. Taken together, our results highlight that PCaP2 plays an important role in chilling tolerance and ABA response by triggering the CBF- and SnRK2-meditated transcriptional regulatory pathways, providing novel evidences of underlying mechanisms of multi-pathways in chilling stress.