Utrecht University, The Netherlands

A plant scientist finds beauty in floral arrangements.

On the face of it, flower arranging is a fiddly affair, and its underlying rules are not immediately obvious to the beholder. But a plant's flowers are always arranged in one of three basic architectures, or 'inflorescences'. These take the form of panicles, loosely but highly branched clusters in which each flower has its own stalk (as in the foxglove); racemes, in which flowers are arranged individually along an unbranched, growing stem (the snapdragon); or cymes, typified by a cluster of branches at the end of a stem that each terminate with flower (the forget-me-not). Simple rules must lie behind this, and simple rules are the foodstuff of mathematical models.

That is the logic behind the work of Przemyslaw Prusinkiewicz at the University of Calgary in Alberta, Canada, and his colleagues. Last year, they published a model in which they imagined that meristems grow into shoots or flowers according to the value of a factor that they named 'veg' (P. Prusinkiewicz et al. Science 316, 1452–1456; 2007). When veg is high, a shoot springs forth; when it is low, a blossom flourishes. Thus, if over time veg decreases at the same rate in all of a plant's growing tips, the model grows a panicle. Other simple rules give rise to a raceme or cyme.

Prusinkiewicz et al. found that, in Arabidopsis, a gene called LEAFY influences the value of veg. But how does this concept apply to plants with different architectures? Recently, Erik Souer of Vrije University in Amsterdam and his collaborators showed that modification of LEAFY activity is crucial for floral architecture in petunia, a cyme, just as the model predicts (E. Souer et al. Plant Cell 20, 2033–2048; 2008). They identify a protein that activates LEAFY only in developing flower buds and that is essential for their architecture. I find the tidy simplicity of these findings more beautiful than any bouquet.

Posted by Anna Petherick at 12:20 PM | Permalink | Comments (0) | TrackBacks (0)

CRP-Santé, Luxembourg

A bioinformatician considers the general applicability of host-pathogen computer simulations

Computer simulations can help explain evolutionary phenomena such as co-evolution and the emergence of robustness. Unlike traditional methods of analysis, such simulations can incorporate detailed representations of environmental antagonisms — such as the pressure that parasites exert on the evolution of their hosts.

This is what Marcel Salathé of ETH Zurich in Switzerland and Orkun Soyer of the University of Trento, Italy, recently analysed at the molecular level. By using computer simulations based on mathematical models, they showed how robust signalling networks may evolve in parasite-infested cells (M. Salathé and O. S. Soyer Mol. Syst. Biol. 4, 202; 2008). In their simulations, signalling networks exhibited increasing redundancy in response to parasites, to the point that a node could be entirely removed without affecting network function. It seems that network redundancy may be a signature of parasitism present or past.

The paper is an exciting invitation to take a computational approach to evolutionary questions, by including more detailed mathematical representations. One could, for example, extend the host-parasite model to incorporate not just protein sequences, but also the ways in which genomic variation is generated, and see how everything plays out.

The approach could be generalized. National security studies, for example, might examine when and how attempts to infiltrate terrorist networks might actually make them more robust. And perhaps Salathé and Soyer's approach could be used to find ways of using environmental interference to reduce the robustness of disease networks, such as cancer signalling pathways, by examining their antagonistic interactions with therapeutic agents.

Posted by Anna Petherick at 12:13 PM | Permalink | Comments (0) | TrackBacks (0)

University College London

Two neuroscientists are surprised by the link between a brain-chemical transporter and sexual orientation.

Many nerve cells in the brain release the chemical neurotransmitter glutamate to signal to other neurons via receptors. Dedicated transporters then remove glutamate from the extracellular space to end signalling.

Cystine–glutamate exchangers are unusual glutamate transporters because they do the reverse, adding glutamate to the extracellular space while removing cystine. David Featherstone of the University of Illinois, Chicago, and his colleagues have found that in the fruitfly Drosophila melanogaster, knocking down expression of a cystine–glutamate exchanger in non-neuronal glial cells leads to a dramatic change in the sexual behaviour of male flies: they mate with both males and females owing to altered processing of sex-specific chemosensory cues (Y. Grosjean et al. Nature Neurosci. 11, 54–61; 2008).

This behaviour may be caused by an increase in the number of glutamate signalling receptors, which is induced by the fall in extracellular glutamate concentration that follows transporter knockdown. Indeed, the effect of the knockdown could be reversed by feeding the flies a drug that reduces glutamate signalling, and could be mimicked by feeding normal flies a drug that enhances glutamate signalling.

These studies raise questions about whether human sexual orientation, long assumed to be due to a mix of genes and environment, could also be altered by perturbations of neurotransmitter signalling. Could differences in such signalling contribute to different sexual preferences?

The possibility of altering sexual preference pharmacologically is worrying. We cannot rule out a future regression to the twentieth-century idea that sexual behaviour should be regulated by society.

Posted by Anna Petherick at 12:12 PM | Permalink | Comments (0) | TrackBacks (0)

Leiden University, the Netherlands

A developmental biologist highlights potential pitfalls of using stem cells that can 'remember' their origins.

For me, embryos are beautiful and their development is endlessly fascinating. They are experts at making new tissues, and accomplish this by using stem cells. Stem cells can develop into mature tissues such as bone or muscle; but, cleverly, some of their progeny remain in an undeveloped state, forming reserve supplies that remain in our bodies into adulthood.

Adult stem cells are found in tissues where cell populations are constantly being renewed, such as the testes, hair follicles and bones. We replace our entire skeleton every decade or so, and rely on stem cells in our bones to do this. Stem cells also have an important role in repair, swinging into action to deal with broken bones and other mishaps.

A recent study in mice yielded remarkable evidence that some of these adult stem cells remember where in the embryo they came from. Jill Helms and her colleagues at Stanford University in California grafted stem cells from one bone into another to see whether they would help repair fractures in the 'wrong' location. Stem cells transplanted from leg bones into fractured jaws failed to produce new bone (P. Leucht et al. Development 135, 2845–2854; 2008). Interestingly, the uncooperative stem cells continued to express a gene, Hoxa11, that acts as a kind of embryonic 'postcode' for the leg.

These findings have broad implications. They validate the concept of non-equivalence — that seemingly identical cells differ if they come from different places in the embryo — first enunciated by Julian Lewis and Lewis Wolpert in the 1970s, and show that it holds in the adult. More pragmatically, if some stem cells also have positional memory, doctors may need to make sure that they take stem cells from the right location to heal damaged tissues.

Posted by Anna Petherick at 12:06 PM | Permalink | Comments (0) | TrackBacks (0)

University of Washington, Seattle

A microbiologist hopes to disrupt bacterial 'decisions'

Cyclic-di-GMP is small but important. It is an intracellular signalling molecule that controls lifestyle choices in bacteria. When should a bacterium become virulent? When should it differentiate into a new cell type? When might it do better to stop moving around and stay still with many others? Bacteria that gather together tend to encase themselves and their neighbours in a carbohydrate slime, forming what is known as a biofilm. I, like many microbiologists, am keen to find ways to disrupt biofilms, and a better understanding of how cyclic-di-GMP works may provide a way to do this.

Recently, answers have started to emerge. First it was shown that cyclic-di-GMP can bind to certain proteins that modulate the activity of flagellar motors — which propel free-swimming bacteria — and to enzymes that make the biofilm-cementing slime. Then researchers found a protein that 'turns on' some of the slime genes when it attaches to cyclic-di-GMP. But one paper shows a completely new way in which cyclic-di-GMP can control bacterial lifestyle choices: by binding to a regulatory region, called a riboswitch, on a messenger RNA molecule (N. Sudarsan et al. Science 321, 411–413; 2008).

Ronald Breaker and his team at Yale University in New Haven, Connecticut, report how they used various molecular-biology techniques to demonstrate that part of the RNA hitches itself to cyclic-di-GMP. They also proved that cyclic-di-GMP-binding riboswitches from several bacterial strains can function as genetic 'off' as well as 'on' switches.

These findings are noteworthy because humans do not make cyclic-di-GMP, so the molecule could be a target for new antibiotics. Medicines that attack cyclic-di-GMP should be able to treat biofilm-related disorders such as periodontal disease and ear infections, which are often resistant to existing drugs.

Posted by Anna Petherick at 12:03 PM | Permalink | Comments (0) | TrackBacks (0)