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N°32 I quarterly I january 2014 Live from the Labs | 9 w ants. This explains why ants tend to ruin only twothirds of the buds: this ratio strikes “a type of balance” that boosts leaf growth without completely threatening their environment. The study not only provides empirical evidence of sanction mechanisms used to keep plant-insect relationships symbiotic instead of turning parasitic, it also helps improve understanding of parasitism in fields such as agronomy or medicine. 01. P.-J.G. Malé et al., “Retaliation in response to castration promotes a low level of virulence in an ant-plant mutualism,” Evol. Biol., 2013. doi:10.1007/ s11692-013-9242-7. 02. Évolution et diversité biologique (Université de Toulouse / Université Paul Sabatier / CNRS / EDB / ENFA). Plants Force Ants to Play Fair by Fui Lee Luk w While many insects and their host plants cohabit in mutually beneficial arrangements, a recent study1 of a French Guianese forest plant (Hirtella physophora) and its guest ants (Allomerus decemarticulatus) shows that such symbiosis is not free from power struggles—and that power does not always flow one way. The researchers were able to describe the plant’s unique retaliation tactic when ants literally nip its flowering process in the bud, exposing how sanction mechanisms can stop one symbiotic partner from dominating the other. In return for shelter in its leaf pouches (pouch-like enlargement at their base) and food nectar, the ants protect the plant by trapping and disabling herbivore Contact information: EDB, Toulouse. Pierre-Jean Malé > pjg.male@gmail.com New Compounds to Treat Cystic Fibrosis BY Clémentin e Wallace w Two newly-discovered chemical compounds could one day be used to treat cystic fibrosis (CF),1 according to a new study led by CNRS researcher Aleksander Edelman.2 CF is a genetic disease caused by mutations in a gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR). Normally, this protein transports anions out of epithelial cells, thereby ensuring correct cellular fluid absorption. However, when CFTR is mutated, fluid absorption is compromised and tissues are not properly hydrated. This causes mucus to accumulate in the lungs, favoring inflammation and infections that are ultimately fatal. In 70% of cases, the disease is caused by one mutation, ΔF508, leading to a misfolded CFTR protein, which is then targeted by housekeeping proteins for degradation. Edelman’s team used computer techniques to screen 200,000 small chemical compounds whose structure might interact with a particular site involved in ΔF508-CFTR recognition by housekeeping proteins. The researchers came up with 12 candidates and selected two that displayed the strongest q The worker ant Allomerus decemarticulatus, cutting a bud of the Hirtella physophora plant. interaction. Treating ΔF508-mutated human cell lines in vitro with these molecules restored some CFTR activity—albeit not to the level of the wild type protein. Increasing the dose of one corrector or using both correctors in synergy increased CFTR activity, suggesting that similar strategies could be used in the clinic. The investigators showed that within the cell, the two correctors hinder the interaction between ΔF508-CFTR and keratin-8, a housekeeping protein involved in the degradation of the mutated protein. ΔF508-CFTR is thereby spared and can perform its function. “The next step is to test whether we can make these compounds more potent and if they can actually protect mice from infections in vivo,” says Edelman. 01. N. Odolczyk et al., “Discovery of novel potent ΔF508-CFTR correctors that target the nucleotide binding domain,” EMBO Mol. Med., 2013. 10: 1484-501. DOI:10.1002/emmm.201302699. 02. Laboratoire Canalopathies épitheliales: la mucoviscidose et autres maladies (CNRS / Inserm / Université Paris Descartes). Biology insects: a win-win situation. “Each partner offers a service and pays a cost,” notes project leader Pierre-Jean Malé of the EDB laboratory.2 The ultimate goal of each, however, is to “cheat and exploit the other, for all forms of mutualism tend toward parasitism,” he adds. In this case, ants betray the Hirtella by chewing up some of its buds, thus forcing it to tap unused flowering energy into growing more leaves—and leaf pouches—to extend ant quarters. To study Hirtella’s reaction to the ants’ abuse, the team compared plants with buds in three states: partially destroyed by ants, protected from ants by a pest barrier, or experimentally cut off. The latter, suffering the harshest damage, showed the fastest growth. But in a surprising twist, these fast growers produced leaf pouches too small to house Plant Biology Contact information: Inserm U806, Paris. Aleksander Edelman > aleksander.edelman@inserm.fr © P.-J. MALE/CNRS Phototh èque Paris Toulouse Control Mutated cells Anti ΔF508-CFTR-K8 Mutated cells + 118208 (1μM) q The red labeling detects the interaction between mutant CFTR and the protein involved in its degradation, K8 (top). Adding the molecule 118208 to mutant cells abolishes this interaction (loss of the red labeling) (bottom). Nuclei are labeled in blue by DAPI. © odolc zyk et al ./embo Molecular Medecine


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