Stomata in the plant epidermis play a critical role in growth and survival by controlling gas exchange, transpiration, and immunity to pathogens. Plants modulate stomatal cell fate and patterning through key transcriptional factors and signaling pathways. MicroRNAs (miRNAs) are known to contribute to developmental plasticity in multicellular organisms; however, no miRNAs appear to target the known regulators of stomatal development. It remains unclear as to whether miRNAs are involved in stomatal development. Here, we report highly dynamic, developmentally stage-specific miRNA expression profiles from stomatal lineage cells. We demonstrate that stomatal lineage miRNAs positively and negatively regulate stomatal formation and patterning to avoid clustered stomata. Target prediction of stomatal lineage miRNAs implicates potential cellular processes in stomatal development. We show that miR399mediated PHO2 regulation, involved in phosphate homeostasis, contributes to the control of stomatal development. Our study demonstrates that miRNAs constitute a critical component in the regulatory mechanisms controlling stomatal development.PHO2 | stomatal development | stomatal lineage miRNA C ontrol of cell lineage and patterning plays a crucial role in the development of multicellular organisms (1-3). Transcription factors can act as master modulators of cell fate specification (2, 4). Environmental factors, including positional cues and neighboring cells, have also been shown to affect cell fate during development (5, 6), indicating developmental flexibility and regulatory complexity in cellular decision making. Genetic reprogramming, including epigenetic regulation and posttranslational modification, consists of multilayers of control and plays a crucial role in the development of cell lineage and patterning (7,8).Stomata are microscopic pores formed by a pair of guard cells (GCs) on the plant epidermis. They govern gas exchange and water loss between plants and the atmosphere. Stomatal functions are tightly regulated as they are critical for photosynthesis and responses to environmental changes. They also play a role in the global ecosystem, affecting atmospheric carbon levels and the global water cycle (9). Stomatal density and distribution affect the functional efficiency of stomata; thus, stomatal development is strictly controlled by developmental and environmental cues to ensure precise stomatal lineage and patterning. For instance, pathogen infection and high temperature reduce stomatal density (10, 11).Stomatal stem cells undergo a series of asymmetric and symmetric cell divisions to form mature GCs. Meristemoid mother cells (MMCs) undergo asymmetric division to produce meristemoids (stomatal entry) that can then undergo additional asymmetric divisions before developing into guard mother cells (GMCs) (commitment). GMCs undergo a single symmetric cell division, and the resultant GCs then differentiate (differentiation) (SI Appendix , Fig. S1A). The stomatal lineage is sequentially regulated by three basic helix-lo...

Leaf senescence is a developmental process designed for nutrient recycling and relocation to maximize growth competence and reproductive capacity of plants. Thus, plants integrate developmental and environmental signals to precisely control senescence. To genetically dissect the complex regulatory mechanism underlying leaf senescence, we identified an early leaf senescence mutant, rse1. RSE1 encodes a putative glycosyltransferase. Loss-of-function mutations in RSE1 resulted in precocious leaf yellowing and up-regulation of senescence marker genes, indicating enhanced leaf senescence. Transcriptome analysis revealed that salicylic acid (SA) and defense signaling cascades were up-regulated in rse1 prior to the onset of leaf senescence. We found that SA accumulation was significantly increased in rse1. The rse1 phenotypes are dependent on SA-INDUCTION DEFICIENT 2 (SID2), supporting a role of SA in accelerated leaf senescence in rse1. Furthermore, RSE1 protein was localized to the cell wall, implying a possible link between the cell wall and RSE1 function. Together, we show that RSE1 negatively modulates leaf senescence through an SID2-dependent SA signaling pathway.

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In this study, cellulose nanoplates (CNPs) were fabricated using cellulose nanocrystals obtained from commercial microcrystalline cellulose (MCC). Their pyrolysis behavior and the characteristics of the product carbonaceous materials were investigated. CNPs showed a relatively high char yield when compared with MCC due to sulfate functional groups introduced during the manufacturing process. In addition, pyrolyzed CNPs (CCNPs) showed more effective chemical activation behavior compared with MCC-induced carbonaceous materials. The activated CCNPs exhibited a microporous carbon structure with a high surface area of 1310.6 m 2 /g and numerous oxygen heteroatoms. The results of this study show the effects of morphology and the surface properties of cellulose-based nanomaterials on pyrolysis and the activation process.

Pluripotent stem cells (PSCs) can serve as an unlimited cell source for transplantation therapies for treating various devastating diseases, such as cardiovascular diseases, diabetes, and Parkinson's disease. However, PSC transplantation has some associated risks, including teratoma formation from the remaining undifferentiated PSCs. Thus, for successful clinical application, it is essential to ablate the proliferative PSCs before or after transplantation. In this study, neural stem cell‐derived conditioned medium (NSC‐CM) inhibited the proliferation of PSCs and PSC‐derived neural precursor (NP) cells without influencing the potential of PSC‐NP cells to differentiate into neurons in vitro and prevented teratoma growth in vivo. Moreover, we found that the NSC‐CM remarkably decreased the expression levels of Oct4 and cyclin D1 that Oct4 directly binds to and increased the cleaved‐caspase 3‐positive cell death through the DNA damage response in PSCs and PSC‐NPs. Interestingly, we found that NSCs distinctly secreted the tissue inhibitor of metalloproteinase (TIMP)‐1 and TIMP‐2 proteins. These proteins suppressed not only the proliferation of PSCs in cell culture but also teratoma growth in mice transplanted with PSCs through inhibition of matrix metalloproteinase (MMP)‐2 and MMP‐9 activity. Taken together, these results suggest that the TIMP proteins may improve the efficacy and safety of the PSC‐based transplantation therapy.