Quantitative law and scenario-based forecasting of different land use expansion, based on reliability analysis in mountainous areas.

The continuous high-intensity and disorderly expansion of construction land in mountainous areas threatens city development; consequently, the scientific guidance of its sustainable development has become a research hotspot. This work aimed to develop a new theoretical framework for predicting land expansion. Based on DMSP/OLS-Landsat 7 data correction from 2000 to 2019, to ensure data reliability, this study quantitatively analysed the expansion law of land-use and land-cover (LULC) in Huayuan, a typical mountainous area in China. Based on the land expansion law, the patch-generating land use simulation (PLUS) model was used to predict various types of LULCs in different scenarios. The results showed that (1) the reliability of LULC under multi-source spatio-temporal data correction reached more than 0.97. (2) The expansion law of industrial and mining land, urban living land, and traffic land is sprawl, while rural living land is enclaved and the expansion direction and intensity are obviously different. (3) The scale of land expansion in the natural-oriented scenario was significantly higher than that in the humanism-oriented scenario, with a higher value of 199.33 hm2. This study expands the case study of land use analysis and prediction, and provides scientific guidance for different land expansion planning, which can avoid the mismatch and waste of land resources. Furthermore, it also deepens the exploration of LULC identification reliability method and enriches the theory of different land use prediction in mountainous areas.

Tak1, Smad4 and Trim33 redundantly mediate TGF-ß3 signaling during palate development.

Transforming growth factor-beta3 (TGF-ß3) plays a critical role in palatal epithelial cells by inducing palatal epithelial fusion, failure of which results in cleft palate, one of the most common birth defects in humans. Recent studies have shown that Smad-dependent and Smad-independent pathways work redundantly to transduce TGF-ß3 signaling in palatal epithelial cells. However, detailed mechanisms by which this signaling is mediated still remain to be elucidated. Here we show that TGF-ß activated kinase-1 (Tak1) and Smad4 interact genetically in palatal epithelial fusion. While simultaneous abrogation of both Tak1 and Smad4 in palatal epithelial cells resulted in characteristic defects in the anterior and posterior secondary palate, these phenotypes were less severe than those seen in the corresponding Tgfb3 mutants. Moreover, our results demonstrate that Trim33, a novel chromatin reader and regulator of TGF-ß signaling, cooperates with Smad4 during palatogenesis. Unlike the epithelium-specific Smad4 mutants, epithelium-specific Tak1:Smad4- and Trim33:Smad4-double mutants display reduced expression of Mmp13 in palatal medial edge epithelial cells, suggesting that both of these redundant mechanisms are required for appropriate TGF-ß signal transduction. Moreover, we show that inactivation of Tak1 in Trim33:Smad4 double conditional knockouts leads to the palatal phenotypes which are identical to those seen in epithelium-specific Tgfb3 mutants. To conclude, our data reveal added complexity in TGF-ß signaling during palatogenesis and demonstrate that functionally redundant pathways involving Smad4, Tak1 and Trim33 regulate palatal epithelial fusion.