Investigating the regulation of the unc-33 promoter by environmental stressors.

Investigating the regulation of the unc-33 promoter by environmental stressors.
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DOI:
10.17912/micropub.biology.000651
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发表时间:
2022
影响因子:
--
通讯作者:
Holgado, Andrea
Holgado, Andrea
中科院分区:
其他
文献类型:
--
作者:
Garcia-Gonzalez, Bianca;Avant, Sarah;Carassco-Pena, Angelica;Miranda, Maria C;Salazar, Kayley;Torres, Eric;Holgado, Andrea

文献摘要

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环境因素,如产前应激,被假设为有助于精神分裂症的发展。Lee和他的同事确定,暴露在产前应激下的大鼠在其前额叶皮质和海马体中只有一种蛋白质DPYSL2的水平降低。DYPSL2是一种在精神分裂症患者中被认为是失活的蛋白质,对神经元发育很重要。线虫DPYSL2的同源物UNC-33也被发现对轴突生长和突触形成至关重要。在这里,我们研究了环境应激源,如温度升高和病原体对UNC-33启动子驱动的GFP表达的影响。结果表明,在暴露于这些产前应激源的线虫中,神经元GFP的表达较低,这使这成为第一个表明UNC-33启动子受环境调节的报告。这项研究为深入了解UNC-33及其与温度和感染相关的表达调控提供了依据。
Environmental factors such as prenatal stress are hypothesized to contribute to the development of schizophrenia. Lee and colleagues determined rats exposed to prenatal stress exhibited decreased levels of only one protein, DPYSL2, in their prefrontal cortex and hippocampus. DYPSL2, a protein seen to be inactivated in schizophrenic patients, is important for neuronal development. The C. elegans homolog of DPYSL2, UNC-33, is also found to be critical for axonal outgrowth and synapse formation. Herein, we study the effects of environmental stressors such as increasing temperatures and pathogens on the expression of GFP driven by the unc-33 promoter. Results indicate that neuronal GFP expression was lower in C. elegans exposed to these prenatal stressors, making this the first report denoting an environmental regulation of the unc -33 promoter. This study provides insight into unc-33 and the regulation of its expression in relation to temperature and infection.