Same Tools, Different Boxes Convergent evolution plays out in plant and animal innate immunity By Philip Hunter As life's diversity demonstrates, nature has a pretty large toolbox for designing adaptations. While in many ways an efficient builder, it often reuses blueprints, even if not starting with the same tools. Analogous wing structures in bird and bat suggest a why-mess-with-success ethos. New World cacti and desert-dwelling Euphorbiaceae in the Old World share protective spines and photosynthesizing stems even though the last common ancestor predates such modifications. Beyond structural adaptations, researchers are investigating convergent evolution at the molecular level, and this may allow for broader comparisons even between plants and animals. Both, of course, share the building blocks and fundamental biochemistry that evolved before the two kingdoms presumably diverged from common single-celled ancestors. But with their radically different cell structures, plants and animals were thought to have pursued largely independent evolutionary routes. Such disparity was reflected in the lack of interaction between the respective research communities. But much is changing, especially with respect to the study of innate immunity, which turns out to involve strikingly similar mechanisms in both plants and animals. One can find resemblances in the receptors that recognize pathogenic components such as lipopolysaccharide; in the signaling systems that initiate responses through kinase cascades; and in the defense mechanisms, including reactive molecules such as nitric oxide, says Jonathan Jones, senior scientist at the Sainsbury Laboratory of the John Innes Centre in Norwich, UK. Moreover, says Jones, autoimmune disorders can develop in plants as well as animals. In many cases, researchers consider plant and animal innate-immunity analogs to have evolved independently, because the underlying genes involved are radically different. Here, convergence is occurring purely at the functional level, according to Daniel Klessig, president and CEO of Boyce Thompson Institute (BTI) for Plant Research in Ithaca, NY. But now, say some, both functional and genetic similarities between plant and animal immunity are leading to cross-pollination between the respective research fields. Read the rest at TheScientist.com http://www.the-scientist.com/yr2004/feb/research4_040216.html Comment: Could viral vectors be suspected here? When the Lights Went On for COP9 A protein's role in ubiquitin-mediated proteasomal degradation plants the seed for big ideas By Eugene Russo It doesn't take a green thumb to predict what happens to plants left in the dark: They wither. But in the late 1980s and early 1990s, researchers, including people in Xing-Wang Deng's Yale University lab, stumbled upon a group of intriguing Arabidopsis mutants that seemed to defy intuition. If provided the right nutrition, these plants could retain a shape, form, and cellular state similar to those grown in ample light for weeks, and even months, of sustained darkness. Some could even flower. In 1994, Deng's group identified COP9, one of the genes responsible for this impressive feat.1 After doing some bioinformatics digging and biochemistry work, they found that the COP9 gene encoded a novel protein that was part of a larger protein complex later called the COP9 signalosome (CSN). As it turns out, the CSN does more than regulate plant responses to light; Deng's lab and others subsequently found signalosome homologs in mammals and other species. "There were a variety of different facts floating around and a lot of speculation," says Svetlana Lyapina, a Hot Paper first author and now a manager of strategy and corporate development at Amgen, Thousand Oaks, Calif. "But there was no sort of unified theory of what signalosome does and how it does it." This issue's Hot Papers2,3 link CSN function to ubiquitin ligases, a family that includes hundreds of known key regulators of inflammation and the cell cycle. Approaching signalosome function from different fields (biochemistry and plant genetics) and with different agendas, the two groups found that in plants,2 yeast, and mammalian cells,3 the CSN directly interacts with an ubiquitin ligase complex that mediates proteasomal degradation of proteins involved in cell cycle and development. "Basically, this provided a biochemical mechanism, a biochemical connection for how COP9 signalosome is involved in protein degradation mediated by the proteasome," says Deng. The complexes are now known to be major signaling processors in the cell, and they may be relevant in treating diseases such as cancer. Thus, with the shade drawn, a new research window had burst open. http://www.the-scientist.com/yr2004/feb/hot_040216.html Posted by Robert Karl Stonjek.
