Burrowing owls and burrowing mammals: are ecosystem engineers interchangeable as facilitators?

Terrestrial vertebrates exhibit dynamic, positive interactions that form and dissolve under different circumstances, usually with multiple species as participants. Ecosystem engineers are important facilitators of other species because they cause physical changes in the environment that alter resource availability. Although a species can be associated with more than one partner, facilitators may not be interchangeable if they differ in abundance, behavioral characteristics, or interactions with other factors in ways that condition the outcome of the association. We examined interactions between burrowing owls (Athene cunicularia) and two burrowing mammals, hairy armadillos (Chaetophractus villosus) and plains vizcachas (Lagostomus maximus), and determined whether these ecosystem engineers are interchangeable for owls. We examined reproductive success for owls nesting in these mammal burrows, constructed a logistic regression model to identify habitat characteristics associated with owl nests, and examined the engineering activities of the mammals. Data on reproduction and habitat indicate that armadillos and vizcachas are not interchangeable for owls. Thirty-five percent of the nests in vizcacha burrows produced fledglings; no fledglings were produced from nests outside vizcachas colonies, even though owls nest successfully in armadillo burrows in other parts of Argentina. Vizcachas facilitate burrowing owls by construction of burrows and by producing open understory vegetation through herbivory. In contrast, armadillos do not alter vegetation, and their burrows are suitable for nest sites only when they occur in recently burned areas or areas maintained by anthropogenic disturbance. Our habitat model also suggests that fire plays a key role in maintaining owl populations because fire is the only natural process that reduces shrubs to the level required by owls. Current management practices of eradication of vizcachas and fire suppression in shrublands could have strong negative consequences for burrowing owls.     

Carboxy Terminal Tail of Polycystin-1 Regulates Localization of TSC2 to Repress mTOR

Autosomal dominant polycystic kidney disease (ADPKD) is a commonly inherited renal disorder caused by defects in the PKD1 or PKD2 genes. ADPKD is associated with significant morbidity, and is a major underlying cause of end-stage renal failure (ESRF). Commonly, treatment options are limited to the management of hypertension, cardiovascular risk factors, dialysis, and transplantation when ESRF develops, although several new pharmacotherapies, including rapamycin, have shown early promise in animal and human studies. Evidence implicates polycystin-1 (PC-1), the gene product of the PKD1 gene, in regulation of the mTOR pathway. Here we demonstrate a mechanism by which the intracellular, carboxy-terminal tail of polycystin-1 (CP1) regulates mTOR signaling by altering the subcellular localization of the tuberous sclerosis complex 2 (TSC2) tumor suppressor, a gatekeeper for mTOR activity. Phosphorylation of TSC2 at S939 by AKT causes partitioning of TSC2 away from the membrane, its GAP target Rheb, and its activating partner TSC1 to the cytosol via 14-3-3 protein binding. We found that TSC2 and a C-terminal polycystin-1 peptide (CP1) directly interact and that a membrane-tethered CP1 protects TSC2 from AKT phosphorylation at S939, retaining TSC2 at the membrane to inhibit the mTOR pathway. CP1 decreased binding of 14-3-3 proteins to TSC2 and increased the interaction between TSC2 and its activating partner TSC1. Interestingly, while membrane tethering of CP1 was required to activate TSC2 and repress mTOR, the ability of CP1 to inhibit mTOR signaling did not require primary cilia and was independent of AMPK activation. These data identify a unique mechanism for modulation of TSC2 repression of mTOR signaling via membrane retention of this tumor suppressor, and identify PC-1 as a regulator of this downstream component of the PI3K signaling cascade.     

Cat gene frequencies in Richmond,California

The frequency of eight mutant genes was sampled and the results compared with studies on other cat populations for various locatities in the U.S.A.     

Genetic control of white flower color in scarlet rosemallow (Hibiscus coccineus Walter)

Scarlet rosemallow (Hibiscus coccineus Walter) is a diploid, perennial, erect, and woody shrub. The species is a desirable inclusion in home landscapes because it is a native plant with attractive flowers and unusual foliage. The objective of these experiments was to determine the number of loci, number of alleles, and gene action controlling flower color (red vs. white) in scarlet rosemallow. Three white-flowered and 1 red-flowered parental lines were used to create S(1) and F(1) populations, which were self-pollinated or backcrossed to generate S(2), F(2), and BC(1) populations. Evaluation of these generations showed that flower color in these populations was controlled by a single diallelic locus with red flower color completely dominant to white. I propose that this locus be named "white flower" with alleles W and w.     

Volatile components of lemur scent secretions vary throughout the year

Olfactory signals can communicate a wide variety of information and are very important in many mammalian species. However, little is known about the olfactory communication of primates. This study used gas chromatography to examine the volatile components of the anogenital gland secretions of wild Milne-Edward's sifaka, Propithecus edwardsi (Primates, Indriidae) (n = 17), captured in Ranomafana National Park, Madagascar. We compared scent swabs of animals and examined differences between social group, age class, sex, and season. The only identified differences in the volatiles were between swabs from the different seasons; all other categories were statistically indistinguishable.     

Activated protein C mediates a healing phenotype in cultured tenocytes

Tendon injuries cause considerable morbidity in the general adult population. The tenocytes within the tendon have the full capacity to heal the tendon intrinsically. Activated protein C (APC) plays an important role in coagulation and inflammation and more recently has been shown to promote cutaneous wound healing. In this study we examined whether APC can induce a wound healing phenotype in tenocytes. Sheep tenocytes were treated with APC, endothelial protein C receptor (EPCR) blocking antibody (RCR252) and/or EPCR small interfering (si)RNA. Cell proliferation and migration were measured by crystal violet assay and a scratch wounding assay, respectively. The expression of EPCR, matrix metalloproteinase (MMP)-2, type I collagen and MAP kinase activity were detected by real time PCR, zymography, immunofluorescence, immunohistochemistry and Western blotting. APC stimulated proliferation, MMP-2 activity and type I collagen deposition in a dose-dependent manner and promoted migration of cultured tenocytes. APC dose-dependently stimulated phosphorylated (P)-ERK2 and inhibited P-p38. Interestingly, tenocytes expressed EPCR protein, which was up-regulated by APC. When tenocytes were pre-treated with RCR252 or EPCR siRNA the effect of APC on proliferation, MMP-2 and type 1 collagen synthesis and MAP kinases was blocked. APC promotes the growth, MMP-2 activity, type I collagen deposition and migration of tenocytes. Furthermore, EPCR is expressed by tenocytes and mediates the actions of APC, at least partly by signalling through selective MAP kinases. These data implicate APC as a potential healing agent for injured tendons.