An invasive tree alters the structure of seed dispersal networks between birds and plants in French Polynesia

Aim We studied how the abundance of the highly invasive fruit‐bearing tree Miconia calvescens DC. influences seed dispersal networks and the foraging patterns of three avian frugivores. Location Tahiti and Moorea, French Polynesia. Methods Our study was conducted at six sites which vary in the abundance of M. calvescens. We used dietary data from three frugivores (two introduced, one endemic) to determine whether patterns of fruit consumption are related to invasive tree abundance. We constructed seed dispersal networks for each island to evaluate how patterns of interaction between frugivores and plants shift at highly invaded sites. Results Two frugivores increased consumption of M. calvescens fruit at highly invaded sites and decreased consumption of other dietary items. The endemic fruit dove, Ptilinopus purpuratus, consumed more native fruit than either of the two introduced frugivores (the red‐vented bulbul, Pycnonotus cafer, and the silvereye, Zosterops lateralis), and introduced frugivores showed a low potential to act as dispersers of native plants. Network patterns on the highly invaded island of Tahiti were dominated by introduced plants and birds, which were responsible for the majority of plant–frugivore interactions. Main conclusions Shifts in the diet of introduced birds, coupled with reduced populations of endemic frugivores, caused differences in properties of the seed dispersal network on the island of Tahiti compared to the less invaded island of Moorea. These results demonstrate that the presence of invasive fruit‐bearing plants and introduced frugivores can alter seed dispersal networks, and that the patterns of alteration depend both on the frugivore community and on the relative abundance of available fruit.     

Direct Regulation of Osteocytic Connexin 43 Hemichannels through AKT Kinase Activated by Mechanical Stimulation

Connexin (Cx) 43 hemichannels in osteocytes are thought to play a critical role in releasing bone modulators in response to mechanical loading, a process important for bone formation and remodeling. However, the underlying mechanism that regulates the opening of mechanosensitive hemichannels is largely unknown. We have recently shown that Cx43 and integrin α5 interact directly with each other, and activation of PI3K appears to be required for Cx43 hemichannel opening by mechanical stimulation. Here, we show that mechanical loading through fluid flow shear stress (FFSS) increased the level of active AKT, a downstream effector of PI3K, which is correlated with the opening of hemichannels. Both Cx43 and integrin α5 are directly phosphorylated by AKT. Inhibition of AKT activation significantly reduced FFSS-induced opening of hemichannels and disrupted the interaction between Cx43 and integrin α5. Moreover, AKT phosphorylation on Cx43 and integrin α5 enhanced their interaction. In contrast to the C terminus of wild-type Cx43, overexpression of the C-terminal mutant containing S373A, a consensus site previously shown to be phosphorylated by AKT, failed to bind with α5 and hence could not inhibit hemichannel opening. Together, our results suggest that AKT activated by FFSS directly phosphorylates Cx43 and integrin α5, and Ser-373 of Cx43 plays a predominant role in mediating the interaction between these two proteins and Cx43 hemichannel opening, a crucial step to mediate the anabolic function of mechanical loading in the bone.     

Inv(10)(p11.2q21.2), a variant chromosome

We present 33 families in which a pericentric inversion of chromosome 10 is segregating. In addition, we summarise the data on 32 families in which an apparently identical inv(10) has been reported in the literature. Ascertainment was through prenatal diagnosis or with a normal phenotype in 21/33 families. In the other 12 families, probands were ascertained through a wide variety of referral reasons but in all but one case (a stillbirth), studies of the family showed that the reason for referral was unrelated to the chromosome abnormality. There has been, to our knowledge, no recorded instance of a recombinant chromosome 10 arising from this inversion and no excess of infertility or spontaneous abortion among carriers of either sex. We propose that inv(10)(p11.2q21.2) can be regarded as a variant analogous to the pericentric inversion of chromosome 2(p11q13). We conclude that prenatal chromosome analysis is not justified for inv(10) carriers. In addition, family investigation of carrier status is not warranted in view of the unnecessary concern this may cause parents and other family members. Received: 7 July 1997 / Accepted: 4 August 1997