Air seeding threshold ( P a ) of xylem vessels from current year growth rings were measured along the vertical axis of mature sugar maple trees ( Acer saccharum Marsh.), with sampling points in primary leaf veins, petioles, 1-, 3-, and 7-year-old branches, large branches, the trunk and roots. The air seeding threshold was taken as the pressure required to force nitrogen gas through intervessel pit membranes. Although all measurements were made on wood produced in the same year, P a varied between different regions of A. saccharum , with distal organs such as leaves and petioles having lower P a than basal regions. Mean (SE) P a ranged from 1.0 ( ± ± ± ± 0.1) MPa in primary leaf veins to 4.8 ( ± ± ± ± 0.1) MPa in the main trunk. Roots exhibited a P a of 2.8 ( ± ± ± ± 0.2) MPa, lower than all other regions of the tree except leaf veins and petioles. Mean xylem vessel diameter increased basipetally, with the widest vessels occurring in the trunk and roots. Within the shoot, wider vessels had greater air seeding thresholds, contrasting with trends previously reported. However, further experimentation revealed that differences in P a between regions of the stem were driven by the presence of primary xylem conduits, rather than differences in vessel diameter. In 1-year-old branches, P a was significantly lower in primary xylem vessels than in adjacent secondary xylem vessels. This explained the lower values of P a measured in petioles and leaf veins, which possessed a greater ratio of primary xylem to secondary xylem than other regions. The difference in P a between primary and secondary xylem was attributed to the greater area of primary cell wall (pit membrane) exposed in primary xylem conduits with helical or annular thickening.

Ecdysis behavior allows insects to shed their old exoskeleton at the end of every molt. It is controlled by a suite of interacting hormones and neuropeptides, and has served as a useful behavior for understanding how bioactive peptides regulate CNS function. Previous findings suggest that crustacean cardioactive peptide (CCAP) activates the ecdysis motor program; the hormone bursicon is believed to then act downstream of CCAP to inflate, pigment, and harden the exoskeleton of the next stage. However, the exact roles of these signaling molecules in regulating ecdysis remain unclear. Here we use a genetic approach to investigate the functions of CCAP and bursicon in Drosophila ecdysis. We show that null mutants in CCAP express no apparent defects in ecdysis and postecdysis, producing normal adults. By contrast, a substantial fraction of flies genetically null for one of the two subunits of bursicon [encoded by the partner of bursicon gene (pburs)] show severe defects in ecdysis, with escaper adults exhibiting the expected failures in wing expansion and exoskeleton pigmentation and hardening. Furthermore, flies lacking both CCAP and bursicon show much more severe defects at ecdysis than do animals null for either neuropeptide alone. Our results show that the functions thought to be subserved by CCAP are partially effected by bursicon, and that bursicon plays an important and heretofore undescribed role in ecdysis behavior itself. These findings have important implications for understanding the regulation of this vital insect behavior and the mechanisms by which hormones and neuropeptides control the physiology and behavior of animals.

Urbanization represents an unintentional global experiment that can provide insights into how species will respond and interact under future global change scenarios. Cities produce many conditions that are predicted to occur widely in the future, such as warmer temperatures, higher carbon dioxide (CO) concentrations and exacerbated droughts. In using cities as surrogates for global change, it is challenging to disentangle climate variables-such as temperature-from co-occurring or confounding urban variables-such as impervious surface-and then to understand the interactive effects of multiple climate variables on both individual species and species interactions. However, such interactions are also difficult to replicate experimentally, and thus the challenges of cities are also their unique advantage. Here, we review insights gained from cities, with a focus on plants and arthropods, and how urban findings agree or disagree with experimental predictions and historical data. We discuss the types of hypotheses that can be best tested in cities, caveats to urban research and how to further validate cities as surrogates for global change. Lastly, we summarize how to achieve the goal of using urban species responses to predict broader regional- and ecosystem-level patterns in the future.

Insect growth is punctuated by molts, during which the animal produces a new exoskeleton. The molt culminates in ecdysis, an ordered sequence of behaviors that causes the old cuticle to be shed. This sequence is activated by Ecdysis triggering hormone (ETH), which acts on the CNS to activate neurons that produce neuropeptides implicated in ecdysis, including Eclosion hormone (EH), Crustacean cardioactive peptide (CCAP) and Bursicon. Despite more than 40 years of research on ecdysis, our understanding of the precise roles of these neurohormones remains rudimentary. Of particular interest is EH; although it is known to upregulate ETH release, other roles for EH have remained elusive. We isolated an Eh null mutant in Drosophila and used it to investigate the role of EH in larval ecdysis. We found that null mutant animals invariably died at around the time of ecdysis, revealing an essential role in its control. Further analyses showed that these animals failed to express the preparatory behavior of pre-ecdysis while directly expressing the motor program of ecdysis. Although ETH release could not be detected, the lack of pre-ecdysis could not be rescued by injections of ETH, suggesting that EH is required within the CNS for ETH to trigger the normal ecdysial sequence. Using a genetically encoded calcium probe, we showed that EH configured the response of the CNS to ETH. These findings show that EH plays an essential role in the Drosophila CNS in the control of ecdysis, in addition to its known role in the periphery of triggering ETH release.