Understanding plant reproductive diversity

Flowering plants display spectacular floral diversity and a bewildering array of reproductive adaptations that promote mating, particularly outbreeding. A striking feature of this diversity is that related species often differ in pollination and mating systems, and intraspecific variation in sexual traits is not unusual, especially among herbaceous plants. This variation provides opportunities for evolutionary biologists to link micro-evolutionary processes to the macro-evolutionary patterns that are evident within lineages. Here, I provide some personal reflections on recent progress in our understanding of the ecology and evolution of plant reproductive diversity. I begin with a brief historical sketch of the major developments in this field and then focus on three of the most significant evolutionary transitions in the reproductive biology of flowering plants: the pathway from outcrossing to predominant self-fertilization, the origin of separate sexes (females and males) from hermaphroditism and the shift from animal pollination to wind pollination. For each evolutionary transition, I consider what we have discovered and some of the problems that still remain unsolved. I conclude by discussing how new approaches might influence future research in plant reproductive biology.     

Random walks and the gas model: spacing behaviour of Grey-Cheeked Mangabeys

1. Simple mechanical models (random walks and the 'gas model') were used to investigate the movement patterns and intergroup encounter rates of a high- and low-density subpopulation of Grey-Cheeked Mangabeys ( Cercocebus albigena johnstoni, Lydeker) at two sites in the Kibale Forest, Western Uganda.
2. Random walk simulations showed that the presence of conspecific groups could act as 'social barriers' which constrained group movements, and promoted high levels of site attachment to a specific home range area.
3. Encounter rate models showed that in the low-density subpopulation (Kanyawara), intergroup encounters occurred no more frequently than expected if groups were moving randomly and independently of each other. This was in contrast to previous analyses which suggested that Grey-Cheeked Mangabeys employed a social spacing mechanism (mediated by male loud calls) in order to reduce the frequency of encounter to below chance levels.
4. Encounters in the high-density subpopulation (Ngogo) were found to occur less frequently than expected at short range (within 100 m). This was suggested to be due to the operation of a territorial mate defence strategy by males at this site.     

The Murray River's 'Sea to Hume Dam' fish passage program: Progress to date and lessons learned

Since its commencement in 2001, a program to facilitate fish passage on a major stretch of Australia's longest river has installed eight structures, testing and modifying their design as they go. What are the results so far and what are the implications for future directions?     

Bone Morphogenetic Protein 7 (BMP-7) Influences Tendon-Bone Integration In Vitro

IntroductionSuccessful graft ingrowth following reconstruction of the anterior cruciate ligament is governed by complex biological processes at the tendon-bone interface. The aim of this study was to investigate in an in vitro study the effects of bone morphogenetic protein 7 (BMP-7) on tendon-bone integration.ResultsIn both models, positive effects of BMP-7 on ALP enzyme activity were observed (p<0.001). Additionally, similar results were noted for LDH activity and lactate concentration. BMP-7 stimulation led to a significant increase in OCN expression. Whereas the effects of BMP-7 on tendon monoculture peaked during an early phase of the experiment (p<0.001), the cocultures showed a maximal increase during the later stages (p<0.001). The histological analysis showed a stimulating effect of BMP-7 on extracellular matrix formation. Organized ossification zones and calcium carbonate-like structures were only observed in the BMP-stimulated cell cultures.DiscussionThis study showed the positive effects of BMP-7 on the biological process of tendon-bone integration in vitro. Histological signs of improved mineralization were paralleled by increased rates of osteoblast-specific protein levels in primary bovine osteoblasts and fibroblasts.ConclusionOur findings indicated a role for BMP-7 as an adjuvant therapeutic agent in the treatment of ligamentous injuries, and they emphasized the importance of the transdifferentiation process of tendinous fibroblasts at the tendon-bone interface.     

Heidenhain's Hematoxylin Used with the Smear Technic

Heidenhain's hematoxylin, according to the following formula, may be used for studying chromosomes in temporary smears of pollen mother cells: 1 part 0.5% hematoxylin and 4% iron-alum (equal parts of each); 1 part 95% alcohol; and 2 parts glacial acetic acid.     

β-Amyloid (Aβ) Oligomers Impair Brain-derived Neurotrophic Factor Retrograde Trafficking by Down-regulating Ubiquitin C-terminal Hydrolase,UCH-L1

We previously found that BDNF-dependent retrograde trafficking is impaired in AD transgenic mouse neurons. Utilizing a novel microfluidic culture chamber, we demonstrate that Aβ oligomers compromise BDNF-mediated retrograde transport by impairing endosomal vesicle velocities, resulting in impaired downstream signaling driven by BDNF/TrkB, including ERK5 activation, and CREB-dependent gene regulation. Our data suggest that a key mechanism mediating the deficit involves ubiquitin C-terminal hydrolase L1 (UCH-L1), a deubiquitinating enzyme that functions to regulate cellular ubiquitin. Aβ-induced deficits in BDNF trafficking and signaling are mimicked by LDN (an inhibitor of UCH-L1) and can be reversed by increasing cellular UCH-L1 levels, demonstrated here using a transducible TAT-UCH-L1 strategy. Finally, our data reveal that UCH-L1 mRNA levels are decreased in the hippocampi of AD brains. Taken together, our data implicate that UCH-L1 is important for regulating neurotrophin receptor sorting to signaling endosomes and supporting retrograde transport. Further, our results support the idea that in AD, Aβ may down-regulate UCH-L1 in the AD brain, which in turn impairs BDNF/TrkB-mediated retrograde signaling, compromising synaptic plasticity and neuronal survival.