RESUMO
The tomato plant (Solanum lycopersicum Mill.) is sensitive to cold, and low field temperatures can result in shortened growth periods and decreased crop yield. Transcription of CRT/DRE-binding factor (CBF) is regulated by INDUCER of CBF EXPRESSION1 (ICE1). CBF activates many downstream genes that confer cold tolerance on plants. ICE1 has been used in genetic engineering to improve cold-resistance in several plant species. Here, ICE1 in a plant expression vector was used to transform a tissue-cultured rhubarb tomato variety using Agrobacterium tumefaciens. The transgenic and control plants were compared at 4°C for 0, 24, and 72 h. We measured leaf physiological indicators related to cold resistance, including malondialdehyde (MDA) and proline (Pro) contents, and peroxidase (POD) and catalase (CAT) activities. At 72 h, the MDA content in transgenic plants was significantly lower than in control plants, indicating a lower membrane lipid injury. The Pro contents and the CAT and POD activities in the transgenic plants increased significantly compared with those of the control plants. For Pro, the increase continued over the prolonged stress exposure, while CAT and POD activities reached peak levels at 24 h. These results are consistent with the roles of Pro, CAT, and POD in defending the integrity of plant cells. Our study not only improves the cold resistance of tomato, but also provides the foundation for further research on the role of ICE1 as a transcription factor in plant cold resistance.
Assuntos
Clonagem Molecular , Proteínas de Plantas/genética , Solanum lycopersicum/genética , Fatores de Transcrição/genética , Transformação Genética , Adaptação Biológica , Temperatura Baixa , Plantas Geneticamente Modificadas , Estresse Fisiológico/genéticaRESUMO
Bladder cancer is a common cancer worldwide and its incidence continues to increase. There are approximately 261,000 cases of bladder cancer resulting in 115,000 deaths annually. This study aimed to integrate bladder cancer genome copy number variation information and bladder cancer gene transcription level expression data to construct a causal-target module network of the range of bladder cancer-related genomes. Here, we explored the control mechanism underlying bladder cancer phenotype expression regulation by the major bladder cancer genes. We selected 22 modules as the initial module network to expand the search to screen more networks. After bootstrapping 100 times, we obtained 16 key regulators. These 16 key candidate regulatory genes were further expanded to identify the expression changes of 11,676 genes in 275 modules, which may all have the same regulation. In conclusion, a series of modules associated with the terms 'cancer' or 'bladder' were considered to constitute a potential network.