Engineering a catabolic pathway in plants for the degradation of 1,2-dichloroethane.

Plants are increasingly being employed to clean up environmental pollutants such as heavy metals; however, a major limitation of phytoremediation is the inability of plants to mineralize most organic pollutants. A key component of organic pollutants is halogenated aliphatic compounds that include 1,2-dichloroethane (1,2-DCA). Although plants lack the enzymatic activity required to metabolize this compound, two bacterial enzymes, haloalkane dehalogenase (DhlA) and haloacid dehalogenase (DhlB) from the bacterium Xanthobacter autotrophicus GJ10, have the ability to dehalogenate a range of halogenated aliphatics, including 1,2-DCA. We have engineered the dhlA and dhlB genes into tobacco (Nicotiana tabacum 'Xanthi') plants and used 1,2-DCA as a model substrate to demonstrate the ability of the transgenic tobacco to remediate a range of halogenated, aliphatic hydrocarbons. DhlA converts 1,2-DCA to 2-chloroethanol, which is then metabolized to the phytotoxic 2-chloroacetaldehyde, then chloroacetic acid, by endogenous plant alcohol dehydrogenase and aldehyde dehydrogenase activities, respectively. Chloroacetic acid is dehalogenated by DhlB to produce the glyoxylate cycle intermediate glycolate. Plants expressing only DhlA produced phytotoxic levels of chlorinated intermediates and died, while plants expressing DhlA together with DhlB thrived at levels of 1,2-DCA that were toxic to DhlA-expressing plants. This represents a significant advance in the development of a low-cost phytoremediation approach toward the clean-up of halogenated organic pollutants from contaminated soil and groundwater.

Progress in understanding the sources, deposition and above-ground fate of trichloroacetic acid.

AIM AND SCOPE: This paper is a companion to the recent review paper by Laturnus et al. (2005) on TCA in soils, presenting a complementary review of knowledge gaps in the sources and fate of trichloroacetic acid (TCA) in plants. MAIN FEATURES: The review considers the various sources of TCA precursors, including the question of how much atmospheric TCA comes from naturally-produced precursors, and addresses the implications of climate change on atmospheric TCA formation. Models of the conversion of precursors to TCA in the atmosphere are critically compared with field measurements of concentrations, deposition and budgets; data on the quantitative relationships between gas-phase TCA, particulate TCA, and TCA dissolved in rain and clouds are reviewed. Methods for quantifying TCA are summarised, along with a description of what the different techniques measure, and how results can be compared. A distinction is made between 'extractable' TCA and 'total' TCA in vegetation. Evidence for the various pathways by which TCA enters plants is given, including the in situ production of TCA in leaves. This leads to a better understanding of how plant tissue concentrations depend on uptake, production and removal rates. Finally, knowledge of the toxic effects of TCA on plants and TCA metabolism in plant tissues is summarised. RESULTS AND DISCUSSION: The discussion highlights knowledge gaps, and is intended to aid the reader in interpreting previously published results through identifying where different ways of expressing data have been used, and the consequent conclusions that can be drawn. CONCLUSION AND FURTHER RESEARCH DIRECTIONS: Recommendations are given for future research directions--in identifying precursor sources, quantifying heterogeneous atmospheric processes, recognising and quantifying uptake pathways, and elucidating the biochemical mechanisms involved in sequestering and degrading TCA inside leaves.