Fruit and nut trees can take as long as two decades to reach maturity, delaying harvesting and limiting the ability of growers to evaluate and breed new strains, with significant economic repercussions. But now, thanks to the tiny weed thale cress (Arabidopsis), orchard trees may one day be blooming and fruiting in the first year of life. A team of researchers in Valencia and Madrid in Spain has exploited two genes from Arabidopsis to engineer orange trees that induce precocious fruit and flowering.
Plant geneticists have identified many of the Arabidopsis genes that regulate flowering initiation and development. Two critical ones, LEAFY (LFY) and APETALA1 (AP1), have previously been shown capable of inducing early flowering when introduced into tobacco, rice, poplar, and aspen (although results were variable). This prompted Leandro Peña and his colleagues to see if they could genetically engineer hybrid orange trees with these genes so that they bloom and produce fruit earlier than their customary five or six years.
When other researchers tried out this system with hybrid aspens and poplars, they got abnormal, infertile flowers only. But the Spanish scientists reasoned that citrus, as a tropical evergreen, would respond to the technique differently than the deciduous aspen. Sure enough, their engineered orange trees dashed through their juvenile phase, produced normal, fertile blossoms, and fruited the first year. What’s more, the precocious characteristics were inherited by offspring of the transgenic trees. The ability to persuade citrus and possibly other woody evergreens to cycle rapidly seems a promising tool for biodiversity and tree-breeding studies, and could have potential economic benefits for fruit growers.
Constitutive expression of Arabidopsis LEAFY or APETALA1 genes in citrus reduces their generation timepp 263 - 267 Leandro Peña, Mar Martín-Trillo, José Juárez, José A. Pina, Luis Navarro & José M. Martínez-Zapater doi:10.1038/85719 Abstract|Full
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A rapid coming of age in tree biotechnologypp 215 - 216 Marcos Egea-Cortines & Julia Weiss doi:10.1038/85641 Abstract|Full
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One of the problems with gene therapy for inherited lung diseases, such as cystic fibrosis, is effectively delivering the therapeutic genes to diseased tissue. Promising gene therapy vectors, such as lentiviruses, used to shuttle genes simply do not penetrate the wall of the lung effectively when inhaled. Help, however, may be on the way from an unlikely source-deadly viruses, such as Ebola virus and influenza virus, which naturally infect the host through the respiratory system. Exploiting the affinity of these viruses for lung tissue, James Wilson and his colleagues have stripped Ebola and influenza of their lung-binding proteins and then engineered them into the coat of a lentiviral gene therapy vector. The resultant vector is much more efficient at delivering genes to lung tissue and holds promise as an agent for the treatment of cystic fibrosis.
To test their system, Wilson and his team studied the efficiency of their hybrid Ebola/lentiviral vector at delivering a test gene-in this instance, a green fluorescent protein that glows green under the microscope-into lung cells in the test tube. They also tested whether the Ebola/lentiviral vector could penetrate the lungs of mice, and also cells lining biopsies of healthy human trachea.
While the hybrid vector appears to be much more effective at gene delivery than other types of vector, it remains to be seen whether vectors containing proteins from deadly pathogens such as Ebola will be appropriate for human use. It is also not clear whether the Ebola/lentiviral vector will be able to penetrate the thick mucus barrier in the lungs of people affected by cystic fibrosis.
Filovirus-pseudotyped lentiviral vector can efficiently and stably transduce airway epithelia in vivopp 225 - 230 Gary P. Kobinger, Daniel J. Weiner, Qian-Chun Yu & James M. Wilson doi:10.1038/85664 Abstract|Full
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The number of infections caused by fungal organisms has increased worldwide in the past decade. Such infections can be quite serious in immunocompromised patients such as those receiving chemotherapy, undergoing organ transplants, or infected with HIV. Unfortunately, the number of antifungal drugs available to treat these infections is limited. In this issue, however, Marianne De Backer and her colleagues have identified genes critical for growth in Candida albicans, a common opportunistic pathogen, and used the genes as potential targets in an antifungal drug screen.
Until now, it has been difficult to identify novel genes in C.albicans that would be useful as targets for antifungal drugs because conventional genetic analysis is stymied by the fungus’s complicated lifecycle. But using information on the C. albicans genome sequence, De Backer’s team has designed a system that can theoretically suppress any of C. albicans complement of genes and test whether those genes are essential for the pathogen’s growth.
By designing synthetic nucleic acids that bind to genes identified in the C. albicans genome sequence, the Belgian team were able to suppress the expression and translation of 86 genes that had a detrimental effect on growth of the fungus. Although half of these genes are of unknown function, many are known to be essential in other organisms, suggesting the approach’s success. In further experiments, the researchers then engineered C. albicans mutants in several of the essential genes and screened them for sensitivity to antifungal drugs. The authors suggest the approach may be adaptable to other similar pathogenic organisms.
An antisense-based functional genomics approach for identification of genes critical for growth of Candida albicanspp 235 - 241 Marianne D. De Backer, Bart Nelissen, Marc Logghe, Jasmine Viaene, Inge Loonen, Sandy Vandoninck, Ronald de Hoogt, Sylviane Dewaele, Fermin A. Simons, Peter Verhasselt, Greet Vanhoof, Roland Contreras & Walter H.M.L. Luyten doi:10.1038/85677 Abstract|Full
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Integrated antifungal drug discovery in Candida albicanspp 212 - 213 Dominique Sanglard doi:10.1038/85634 Abstract|Full
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In Europe and North America, potatoes are eaten mostly as greasy snacks in the form of chips or fries. What most people don’t realize is that potatoes-when compared with rice, corn, or wheat-are extremely rich in protein, vitamin C, and calcium, and are the primary staple food in Latin America and areas of Southeast Asia. The potato would be an even more useful crop if it weren’t for the unpredictable timing of sprouting when in storage or transportation. Creating potatoes that sprout sooner could help in regions where two potato crops are grown each year; where infection during dormancy is prevalent; and where seed potatoes are exported between regions of different climate. In this issue, scientists at the Max Planck Institute for Molecular Plant Physiology led by Eva Farré describe potatoes that have been genetically modified to sprout seven weeks earlier than their wild-type counterparts.
Farré’s team posited that the sprouting of potatoes is initiated by starch breakdown and subsequent formation of various metabolites required for growth. Knowing that pyrophosphate plays a central role in starch degradation and sucrose synthesis, they generated transgenic potatoes expressing in their tubers a bacterial enzyme that breaks down pyrophosphate (pyrophosphatase). The resulting GM potatoes exhibited a reduction in pyrophosphate and a resultant increase in starch breakdown and sucrose production. These potatoes sprouted 15 weeks after planting, 7 weeks earlier than the wild-type. The trait was also passed on to subsequent generations suggesting that the pyrophosphatase was stable in the potato DNA.
The knowledge gained by this research could someday result in GM potatoes with delayed sprouting, which would enable longer-term storage and transport of the tubers.
Acceleration of potato tuber sprouting by the expression of a bacterial pyrophosphatasepp 268 - 272 Eva M. Farré, Antje Bachmann, Lothar Willmitzer & Richard N. Trethewey doi:10.1038/85726 Abstract|Full
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