SOIL ALUMINUM TOLERANCE BY MYCORRHIZAL & NON MYCORRHIZAL PINES: HEAVY METALS

菌根对土壤铝的耐受性

• 批准号: 6493748
• 负责人: JANET MACFALL
• 金额: $ 28.8万
• 依托单位: DUKE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2001
• 资助国家: 美国
• 起止时间: 2001-09-01 至 2002-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6493748
• 关键词: Mammalia; biomedical resource; cardiovascular system; genetics; growth /development; human tissue; model design /development; nuclear magnetic resonance spectroscopy

Cardiovascular defects are the most common defects in human infants, affecting one of two hundred live births. Although many of these cardiac malformations have well defined phenotypes, currently very few candidate genes have been identified as playing a role in these heart malformations. Recent studies suggest that the connexin 43 (Cx43) gap junction gene may be one such candidate gene. Cx43 knockout (KO) mice die at birth as a result of conotruncal defects associated with pulmonary stenosis and ventricular septal defects. Given that previous ablation studies have shown the importance of occipital neural crest cells in conotruncal development, we suggest that perturbation of neural crest cells may underlie the cardiovascular malformations resulting from Cx43 perturbation. Consistent with this possibility is the fact that neural crest cells express the Cx43 gap junction gene, and are functionally coupled via gap junctions. Furthermore, Cx43 expression in the CMV43 transgenic mice is driven by the cytomegaloviral promoter, a promoter which restricts transgene expression to the dorsal neural tube, and a subpopulation of neural crest cells, including neural crest cells that migrate to the heart outflow tract. In light of these observations, we propose experiments to further examine whether perturbation of neural crest cells may underlie the cardiovascular malformations seen in mice harboring the loss of Cx43 function. We will characterize cardiovascular morphogenesis in the Cx43 KO and CMV43 transgenic mice using histology, echocardiography, and MRI analyses. We will perform echocardiography on live embryos (in-utero), send the pregnant female to Duke, perfuse the embryos with BSA-DTPA-Gd, perform a quick survey scan of each embryo, and then perform a 3D spin echo scan on homozygote KO embryos that looked promising in the survey scans. We anticipate preparing 4 litters of embryos, and performing 3D scans on 6-8 of the embryos on the 9T magnet.

心血管缺陷是人类最常见的缺陷 婴儿，影响200个活产婴儿中的一个。 虽然许多 这些心脏畸形具有明确的表型， 很少有候选基因被确定为在以下方面起作用： 这些心脏畸形 最近的研究表明，连接蛋白 43（Cx43）间隙连接基因可能是这样一个候选基因。 Cx43 敲除（KO）小鼠在出生时由于圆锥动脉干缺陷而死亡 与肺动脉狭窄和室间隔缺损有关。 鉴于先前的消融研究已经表明 枕神经嵴细胞在锥体干发育中的作用，我们认为 神经嵴细胞的扰动可能是 Cx43干扰导致的心血管畸形。 与这种可能性相一致的是， 表达Cx43间隙连接基因，并通过 缝隙连接 此外，CMV 43转基因细胞中Cx43的表达也与CMV 43转基因细胞中Cx43的表达有关。 小鼠是由巨细胞病毒启动子驱动的，该启动子 将转基因表达限制在背神经管， 神经嵴细胞的亚群，包括 迁移到心脏流出道。 根据这些观察， 我们提出实验，以进一步研究是否扰动的 神经嵴细胞可能是心血管畸形的基础 在Cx43功能缺失的小鼠中。 我们将描述 Cx43 KO和CMV 43转基因小鼠的心血管形态发生 通过组织学超声心动图和核磁共振分析 我们将执行 活胚胎超声心动图（子宫内），将妊娠女性 给杜克注射BSA-DTPA-Gd 扫描每个胚胎，然后进行3D自旋回波扫描， 在调查扫描中看起来有希望的纯合子KO胚胎。 我们 预计准备4窝胚胎，并进行3D扫描， 6-8 9 T磁铁上的胚胎