Canopy structure of bahiagrass (Paspalum notatum Flügge) swards was analyzed in terms of accessibility and availability of individual leaves on a tiller. Tillers in swards under three nitrogen rates (0, 12 and 24 g m−2 year−1) × two cutting heights (3 and 10 cm above ground level) were measured in May (spring), July (summer) and October (autumn), for the heights of the basal and the highest point and the dry matter (DM) weights of individual leaves (laminae; L1, L2, L3 and so on; L1 = the uppermost or the youngest lamina) and a stem (inclusive of leaf sheaths). The tillers were relatively short in May and October and tall in July, having 10, six and seven leaves, respectively. The leaves were almost always green (no dry part) until L5 in May and until L4 in July and October. In each season, the relative accessibility (height rank of the maximum point) and availability (weight rank) of the leaves on the tiller was almost constant across the nitrogen rates and cutting heights, showing L1–L4 to be highly accessible and L3–L5 and L2 or L6 to be highly available (top four leaves). L3 was almost always the most accessible and available leaf across the seasons and the treatments, followed by L4 and L2. The results indicate the usefulness of the constant relative accessibility and availability of individual leaves on the tiller in the management and modeling of bahiagrass swards.
Vestigial‐like family member 3 (VGLL3) is a cofactor for TEA domain transcription factors (TEADs). Although VGLL3 is known to be highly expressed and stimulate cell proliferation in mesenchymal cancer cells, its involvement in mesenchymal phenotypes is largely unknown. In this study, we found that VGLL3 promotes epithelial‐to‐mesenchymal transition (EMT)‐like phenotypic changes. We found that A549 human lung cancer cells stably expressing VGLL3 exhibit spindle‐like morphological changes, reduction in the epithelial marker E‐cadherin and induction of the mesenchymal marker Snail. Notably, VGLL3‐expressing cells exhibited enhanced motility. The DNA‐binding protein high‐mobility group AT‐hook 2 (HMGA2) was found to be a target of the VGLL3‐TEAD4 complex, and HMGA2 knockdown repressed EMT‐like phenotypic changes in VGLL3‐expressing cells. VGLL3‐dependent phenotypic changes are involved in transforming growth factor‐β (TGF‐β)‐induced EMT progression. VGLL3 or HMGA2 knockdown repressed the motility of the mesenchymal breast cancer MDA‐MB‐231 cells. Importantly, high levels of VGLL3 expression were shown to have a positive correlation with poor prognosis in various human cancers, such as breast, colon, ovarian, head and neck, pancreatic, renal, gastric and cervical cancers. These results suggest that VGLL3 promotes EMT‐like cell motility by inducing HMGA2 expression and accelerates cancer progression.
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