Closely related bird species demonstrate flexibility between beak morphology and underlying developmental programs.

The astonishing variation in the shape and size of bird beaks reflects a wide range of dietary specializations that played an important role in avian diversification. Among Darwin's finches, ground finches (Geospiza spp.) have beaks that represent scaling variations of the same shape, which are generated by alterations in the signaling pathways that regulate growth of the two skeletal components of the beak: the prenasal cartilage (pnc) and the premaxillary bone (pmx). Whether this developmental mechanism is responsible for variation within groups of other closely related bird species, however, has remained unknown. Here, we report that the Caribbean bullfinches (Loxigilla spp.), which are closely related to Darwin's finches, have independently evolved beaks of a novel shape, different from Geospiza, but also varying from each other only in scaling. However, despite sharing the same beak shape, the signaling pathways and tissues patterning Loxigilla beaks differ among the three species. In Loxigilla noctis, as in Geospiza, the pnc develops first, shaped by Bmp4 and CaM signaling, followed by the development of the pmx, regulated by TGFßIIr, ß-catenin, and Dkk3 signaling. In contrast, beak morphogenesis in Loxigilla violacea and Loxigilla portoricensis is generated almost exclusively by the pmx through a mechanism in which Ihh and Bmp4 synergize to promote expansion of bone tissue. Together, our results demonstrate high flexibility in the relationship between morphology and underlying developmental causes, where different developmental programs can generate identical shapes, and similar developmental programs can pattern different shapes.

A universal growth limit for circular lichens.

Lichens fix carbon dioxide from the air to build biomass. Crustose and foliose lichens grow as nearly flat, circular disks. Smaller individuals grow slowly, but with small, steady increases in radial growth rate over time. Larger individuals grow more quickly and with a roughly constant radial velocity maintained over the lifetime of the lichen. We translate the coffee drop effect to model lichen growth and demonstrate that growth patterns follow directly from the diffusion of carbon dioxide in the air around a lichen. When a lichen is small, carbon dioxide is fixed across its surface, and the entire thallus contributes to radial growth, but when a lichen is larger carbon dioxide is disproportionately fixed at the edges of an individual, which are the primary drivers of growth. Tests of the model against data suggest it provides an accurate, robust, and universal framework for understanding the growth dynamics of both large and small lichens in nature.

Shared developmental programme strongly constrains beak shape diversity in songbirds.

The striking diversity of bird beak shapes is an outcome of natural selection, yet the relative importance of the limitations imposed by the process of beak development on generating such variation is unclear. Untangling these factors requires mapping developmental mechanisms over a phylogeny far exceeding model systems studied thus far. We address this issue with a comparative morphometric analysis of beak shape in a diverse group of songbirds. Here we show that the dynamics of the proliferative growth zone must follow restrictive rules to explain the observed variation, with beak diversity constrained to a three parameter family of shapes, parameterized by length, depth and the degree of shear. We experimentally verify these predictions by analysing cell proliferation in the developing embryonic beaks of the zebra finch. Our findings indicate that beak shape variability in many songbirds is strongly constrained by shared properties of the developmental programme controlling the growth zone.

A natural O-ring optimizes the dispersal of fungal spores.

The forcibly ejected spores of ascomycete fungi must penetrate several millimetres of nearly still air surrounding sporocarps to reach dispersive airflows, and escape is facilitated when a spore is launched with large velocity. To launch, the spores of thousands of species are ejected through an apical ring, a small elastic pore. The startling diversity of apical ring and spore shapes and dimensions make them favoured characters for both species descriptions and the subsequent inference of relationships among species. However, the physical constraints shaping this diversity and the adaptive benefits of specific morphologies are not understood. Here, we develop an elastohydrodynamic theory of the spore's ejection through the apical ring and demonstrate that to avoid enormous energy losses during spore ejection, the four principal morphological dimensions of spore and apical ring must cluster within a nonlinear one-dimensional subspace. We test this prediction using morphological data for 45 fungal species from two different classes and 18 families. Our sampling encompasses multiple loss and gain events and potentially independent origins of this spore ejection mechanism. Although the individual dimensions of the spore and apical ring are only weakly correlated with each other, they collapse into the predicted subspace with high accuracy. The launch velocity appears to be within 2 per cent of the optimum for over 90 per cent of all forcibly ejected species. Although the morphological diversity of apical rings and spores appears startlingly diverse, a simple principle can be used to organize it.

Murine Nod1 but not its human orthologue mediates innate immune detection of tracheal cytotoxin.

Tracheal cytotoxin (TCT) was originally described as the minimal effector that was able to reproduce the cytotoxic response of Bordetella pertussis on ciliated epithelial cells. This molecule triggers pleiotropic effects such as immune stimulation or slow-wave sleep modulation. Further characterization identified TCT as a specific diaminopimelic acid (DAP)-containing muropeptide, GlcNAc-(anhydro)MurNAc-L-Ala-D-Glu-mesoDAP-D-Ala. Here, we show that the biological activity of TCT depends on Nod1, an intracellular sensor of bacterial peptidoglycan. However, Nod1-dependent detection of TCT was found to be host specific, as human Nod1 (hNod1) poorly detected TCT, whereas mouse Nod1 (mNod1) did so efficiently. More generally, hNod1 required a tripeptide (L-Ala-D-Glu-mesoDAP) for efficient sensing of peptidoglycan, whereas mNod1 detected a tetrapeptide structure (L-Ala-D-Glu-mesoDAP-D-Ala). In murine macrophages, TCT stimulated cytokine secretion and NO production through Nod1. Finally, in vivo, injection of the tetrapeptide structure in mice triggered a transient yet strong release of cytokines into the bloodstream and the maturation of macrophages, in a Nod1-dependent manner. This study thereby identifies Nod1 as the long sought after sensor of TCT in mammals.