Aliphatic alcohols naturally exist in many organisms as important cellular components; however, their roles in extracellular polymer biosynthesis are poorly defined. We report here the isolation and characterization of a rice (Oryza sativa) malesterile mutant, defective pollen wall (dpw), which displays defective anther development and degenerated pollen grains with an irregular exine. Chemical analysis revealed that dpw anthers had a dramatic reduction in cutin monomers and an altered composition of cuticular wax, as well as soluble fatty acids and alcohols. Using map-based cloning, we identified the DPW gene, which is expressed in both tapetal cells and microspores during anther development. Biochemical analysis of the recombinant DPW enzyme shows that it is a novel fatty acid reductase that produces 1-hexadecanol and exhibits >270-fold higher specificity for palmiltoyl-acyl carrier protein than for C16:0 CoA substrates. DPW was predominantly targeted to plastids mediated by its N-terminal transit peptide. Moreover, we demonstrate that the monocot DPW from rice complements the dicot Arabidopsis thaliana male sterile2 (ms2) mutant and is the probable ortholog of MS2. These data suggest that DPWs participate in a conserved step in primary fatty alcohol synthesis for anther cuticle and pollen sporopollenin biosynthesis in monocots and dicots.
MiR‐140 is a microRNA specially involved in chondrogenesis and osteoarthritis pathogenesis. However, its transcriptional regulation and target genes in cartilage development are not fully understood. Here we detected that miR‐140 was uniquely expressed in chondrocyte and suppressed by Wnt/β‐catenin signalling. The miR‐140 primary transcript was an intron‐retained RNA co‐expressed with Wwp2‐C isoform, which was directly induced by Sox9 through binding to the intron 10 of Wwp2 gene. Knockdown of miR‐140 in limb bud micromass cultures resulted in arrest of chondrogenic proliferation. Sp1, the activator of the cell cycle regulator p15INK4b, was identified as a target of miR‐140 in maintaining the chondrocyte proliferation. Collectively, our findings expand our understanding of the transcriptional regulation and the chondrogenic role of miR‐140 in chondrogenesis.
Airway epithelial cells (AECs) are part of the frontline defense against infection of pathogens by providing both a physical barrier and immunological function. The role of AECs in the innate and adaptive immune responses, through the production of antimicrobial molecules and proinflammatory factors against a variety of pathogens, has been well established. Tuberculosis (TB), a contagious disease primarily affecting the lungs, is caused by the infection of various strains of mycobacteria. In response to mycobacteria infection, epithelial expression of Toll-like receptors and surfactant proteins plays the most prominent roles in the recognition and binding of the pathogen, as well as the initiation of the immune response. Moreover, the antimicrobial substances, proinflammatory factors secreted by AECs, composed a major part of the innate immune response and mediation of adaptive immunity against the pathogen. Thus, a better understanding of the role and mechanism of AECs in response to mycobacteria will provide insight into the relationship of epithelial cells and lung immunocytes against TB, which may facilitate our understanding of the pathogenesis and immunological mechanism of pulmonary tuberculosis disease.
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