ABSTRACT
Land use (LU) changes caused by urbanization, climate, and anthropogenic activities alter the supply of ecosystem services (ES), which affects the ecological service value (ESV) of a given region. Existing LU simulation models extract neighborhood effects with only one data time slice, which ignores long-term dependence in neighborhood interactions. Previous studies on the dynamic relationship between LU change and ES in semi-arid areas is rare than that in humid coastal areas. Here, we selected a semi-arid city, Lanzhou, in Northwest China as the study area, to simulate LU changes in 2030 under natural growth (NG), ecological protection (EP), economic development (EP), and ecological protection-economic development (EPD) scenarios, using a novel deep learning method, named CL-CA. Convolutional neural network and long short term memory (CNN-LSTM) with cellular automata (CA) were utilized to extract the spatiotemporal neighborhood features. The overall simulation performance of the proposed model was larger than 0.92, which is surpassed that of LSTM-CA, artificial neural network (ANN)-CA, and recursive neural network (RNN)-CA. Ultimately, we utilized LU and ES to quantitatively evaluate the ESV changes. The results indicated that: (1) The variable trend of ESV in arid area is different from that in coastal humid areas. (2) Forest land and water were the main factors that affect the ESV change. (3) The EPD scenario was more suitable for sustainable urban development.
Subject(s)
Deep Learning , Ecosystem , China , Conservation of Natural Resources , UrbanizationABSTRACT
Olenecamptus bilobus Fabricius is widely distributed in some parts of Southeast and East Asia whose larvae bore under the bark of at least eleven plant families. The complete mitochondria genome of O. bilobus was 15,262 bp in length, with 37 genes, including 12 protein-coding genes (PCGs), 23 tRNA genes (tRNAs), and 2 rRNA genes (rRNAs). The A + T content is 76.91%, showing strong AT skew. Phylogenetic analysis indicated that O. bilobus had a close relationship with Olenecamptus subobliteratus Pic.
ABSTRACT
Epipedocera atra is a common species of Epipedocera Chevrolat which distributed in South China and some countries in Southeast Asia. The complete mitochondria genome of E. atra was 15,662 bp in length, with 37 genes, including 13 protein-coding genes (PCGs), 22 tRNA genes (tRNAs), and 2 rRNA genes (rRNAs). The nucleotide composition was highly A + T biased, accounting for 70.34% of the whole mitogenome. Phylogenetic analysis indicated that E. atra had a close relationship with Xylotrechus grayii White.
ABSTRACT
RASSF7 protein localises to the centrosome and plays a key role in mitosis. Its expression is also increased in a range of tumour types. However, little is known about the molecular basis of RASSF7's function and it is not clear if it acts as an oncogene in the cancers where its levels are elevated. Here, we carry out the first analysis of the domains of rassf7, focusing on which of them are responsible for its localisation to the centrosome. Constructs were generated to allow the expression of a series of truncated versions of rassf7 and the level of centrosomal localisation shown by each protein quantified. This analysis was carried out in Xenopus embryos which are a tractable system where rassf7 localisation can easily be studied. Our data shows that the coiled-coil domain of rassf7 is required and sufficient to direct its centrosomal localisation. The RA domain did not appear to have a role in mediating localisation. Surprisingly, removal of the extreme C-terminus of the protein caused rassf7 to accumulate at the centrosome and drive centrosome defects, including accumulation of the centrosomal protein γ-tubulin and an amplification of the number of γ-tubulin foci. These effects required the centrosomal localisation mediated by the coiled-coil domain. Later in development cells expressing this truncated rassf7 protein underwent cell death. Finally, analysis of a database of tumour sequences identified a mutation in RASSF7 which would cause a similar C-terminal truncation of the protein. Based on our data this truncated protein might drive centrosomal defects and we propose the hypothesis that truncated RASSF7 could act as an oncogene in a small subset of tumours where it is mutated in this way.