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The tremendous personal and economic burden worldwide caused by low back pain (LBP) has been surging in recent years. While intervertebral disc degeneration (IVDD) is the leading cause of LBP and vast efforts have been made to develop effective therapies, this problem is far from being resolved, as most treatments, such as painkillers and surgeries, mainly focus on relieving the symptoms rather than reversing the cause of IVDD. However, as stem/progenitor cells possess the potential to regenerate IVD, a deeper understanding of the early development and role of these cells could help to improve the effectiveness of stem/progenitor cell therapy in treating LBP. Single-cell RNA sequencing results provide fresh insights into the heterogeneity and development patterns of IVD progenitors; additionally, we compare mesenchymal stromal cells and IVD progenitors to provide a clearer view of the optimal cell source proposed for IVD regeneration. [ABSTRACT FROM AUTHOR]

Mitogen‐activated protein kinases (MPKs) play essential roles in guard cell signaling, but whether MPK cascades participate in guard cell ethylene signaling and interact with hydrogen peroxide (H2O2), nitric oxide (NO), and ethylene‐signaling components remain unclear. Here, we report that ethylene activated MPK3 and MPK6 in the leaves of wild‐type Arabidopsis thaliana as well as ethylene insensitive2 (ein2), ein3, nitrate reductase1 (nia1), and nia2 mutants, but this effect was impaired in ethylene response1 (etr1), nicotinamide adenine dinucleotide phosphate oxidase AtrbohF, mpk kinase1 (mkk1), and mkk3 mutants. By contrast, the constitutive triple response1 (ctr1) mutant had constitutively active MPK3 and MPK6. Yeast two‐hybrid, bimolecular fluorescence complementation, and pull‐down assays indicated that MPK3 and MPK6 physically interacted with MKK1, MKK3, and the C‐terminal region of EIN2 (EIN2 CEND). mkk1, mkk3, mpk3, and mpk6 mutants had typical levels of ethylene‐induced H2O2 generation but impaired ethylene‐induced EIN2 CEND cleavage and nuclear translocation, EIN3 protein accumulation, NO production in guard cells, and stomatal closure. These results show that the MKK1/3–MPK3/6 cascade mediates ethylene‐induced stomatal closure by functioning downstream of ETR1, CTR1, and H2O2 to interact with EIN2, thereby promoting EIN3 accumulation and EIN3‐dependent NO production in guard cells. [ABSTRACT FROM AUTHOR]