Recent studies provide evidence that premature maternal decidual senescence resulting from heightened mTORC1 signaling is a cause of preterm birth (PTB). We show here that mice devoid of fatty acid amide hydrolase (FAAH) with elevated levels of N-arachidonyl ethanolamide (anandamide), a major endocannabinoid lipid mediator, were more susceptible to PTB upon lipopolysaccharide (LPS) challenge. Anandamide is degraded by FAAH and primarily works by activating two G-protein-coupled receptors CB1 and CB2, encoded by Cnr1 and Cnr2, respectively. We found that Faah^−/− decidual cells progressively underwent premature senescence as marked by increased senescence-associated β-galactosidase (SA-β-Gal) staining and γH2AX-positive decidual cells. Interestingly, increased endocannabinoid signaling activated MAPK p38, but not p42/44 or mTORC1 signaling, in Faah^−/− deciduae, and inhibition of p38 halted premature decidual senescence. We further showed that treatment of a long-acting anandamide in wild-type mice at midgestation triggered premature decidual senescence utilizing CB1, since administration of a CB1 antagonist greatly reduced the rate of PTB in Faah^−/− females exposed to LPS. These results provide evidence that endocannabinoid signaling is critical in regulating decidual senescence and parturition timing. This study identifies a previously unidentified pathway in decidual senescence, which is independent of mTORC1 signaling.

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.

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 β-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.