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Transgenic Nicotiana tabacum with tolerance to 2,4-D has previously been produced using a bacterial 2,4-D-dioxygenase gene (tfdA) driven by the 35S promoter of cauliflower mosaic virus. Using promoters from the Pisum sativum plastocyanin gene (petE) and an Arabidopsis thaliana histone gene (H4A), we demonstrate that similar protection from 2,4-D can be obtained in transgenic N. tabacum by targeting expression of tfdA to either meristematic tissues or chloroplast-containing tissues. As with the 35S promoter constructs, the plants are tolerant but not completely resistant; very young seedlings in particular are only slightly protected. However, the levels of tolerance observed could offer a useful degree of protection from accidental spray drift.
Genetic studies in animal models have started to open new ways for understanding the underlying molecular pathophysiology of hydrocephalus. Human hydrocephalus can be classified as syndromic versus non-syndromic, and congenital versus acquired. Comparative twin studies have been performed to analyze the genetic influences in congenital structural defects including hydrocephalus. Familial hydrocephalus has long been suggested as a heritable disease, with heterogeneous causes, which may result from distinct monogenic or multifactorial disorders. Congenital hydrocephalus (CHC) is usually the consequence of deficient brain development and perturbed cellular function, implicating the important roles that CHC genes play during brain development. The majority of identified hydrocephalus loci and genes are from genetic analysis in hydrocephalic animal models. The pathophysiology of hydrocephalus in the ventricular system has been extensively studied through either down- or up-regulation of certain targeted gene expression, followed by comparative morphological and molecular studies.
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