Earliest Mexican Turkeys (Meleagris gallopavo) in the Maya Region: Implications for Pre-Hispanic Animal Trade and the Timing of Turkey Domestication

Late Preclassic (300 BC-AD 100) turkey remains identified at the archaeological site of El Mirador (Petén, Guatemala) represent the earliest evidence of the Mexican turkey (Meleagris gallopavo) in the ancient Maya world. Archaeological, zooarchaeological, and ancient DNA evidence combine to confirm the identification and context. The natural pre-Hispanic range of the Mexican turkey does not extend south of central Mexico, making the species non-local to the Maya area where another species, the ocellated turkey (Meleagris ocellata), is indigenous. Prior to this discovery, the earliest evidence of M. gallopavo in the Maya area dated to approximately one thousand years later. The El Mirador specimens therefore represent previously unrecorded Preclassic exchange of animals from northern Mesoamerica to the Maya cultural region. As the earliest evidence of M. gallopavo found outside its natural geographic range, the El Mirador turkeys also represent the earliest indirect evidence for Mesoamerican turkey rearing or domestication. The presence of male, female and sub-adult turkeys, and reduced flight morphology further suggests that the El Mirador turkeys were raised in captivity. This supports an argument for the origins of turkey husbandry or at least captive rearing in the Preclassic.     

Asynchronous origins of ectomycorrhizal clades of Agaricales

The ectomycorrhizal (ECM) symbiosis is the most widespread biotrophic nutritional mode in mushroom-forming fungi. ECM fungi include, though are not limited to, about 5000 described species of Agaricales from numerous, independently evolved lineages. Two central hypotheses suggest different explanations for the origin of ECM fungal diversity: (i) dual origins, initially with the Pinaceae in the Jurassic and later with angiosperms during the Late Cretaceous, and (ii) a simultaneous and convergent radiation of ECM lineages in response to cooling climate during the Palaeogene and advancing temperate ECM plant communities. Neither of these hypotheses is supported here. While we demonstrate support for asynchronous origins of ECM Agaricales, the timing of such events appears to have occurred more recently than suggested by the first hypothesis, first during the Cretaceous and later during the Palaeogene. We are also unable to reject models of rate constancy, which suggests that the diversity of ECM Agaricales is not a consequence of convergent rapid radiations following evolutionary transitions from saprotrophic to ECM habits. ECM lineages of Agaricales differ not only in age, but also in rates of diversification and rate of substitution at nuclear ribosomal RNA loci. These results question the biological uniformity of the ECM guild.     

Non-invasive measurements of exhaled NO and CO associated with methacholine responses in mice

Background

Nitric oxide (NO) and carbon monoxide (CO) in exhaled breath are considered obtainable biomarkers of physiologic mechanisms. Therefore, obtaining their measures simply, non-invasively, and repeatedly, is of interest, and was the purpose of the current study.

Methods

Expired NO (E_NO) and CO (E_CO) were measured non-invasively using a gas micro-analyzer on several strains of mice (C57Bl6, IL-10^-/-, A/J, MKK3^-/-, JNK1^-/-, NOS-2^-/- and NOS-3^-/-) with and without allergic airway inflammation (AI) induced by ovalbumin systemic sensitization and aerosol challenge, compared using independent-sample t-tests between groups, and repeated measures analysis of variance (ANOVA) within groups over time of inflammation induction. E_NO and E_CO were also measured in C57Bl6 and IL-10-/- mice, ages 8–58 weeks old, the relationship of which was determined by regression analysis. S-methionyl-L-thiocitrulline (SMTC), and tin protoporphyrin (SnPP) were used to inhibit neuronal/constitutive NOS-1 and heme-oxygenase, respectively, and alter NO and CO production, respectively, as assessed by paired t-tests. Methacholine-associated airway responses (AR) were measured by the enhanced pause method, with comparisons by repeated measures ANOVA and post-hoc testing.

Results

E_NO was significantly elevated in naïve IL-10^-/- (9–14 ppb) and NOS-2^-/- (16 ppb) mice as compared to others (average: 5–8 ppb), whereas E_CO was significantly higher in naïve A/J, NOS-3^-/- (3–4 ppm), and MKK3^-/- (4–5 ppm) mice, as compared to others (average: 2.5 ppm). As compared to C57Bl6 mice, AR of IL-10^-/-, JNK1^-/-, NOS-2^-/-, and NOS-3^-/- mice were decreased, whereas they were greater for A/J and MKK3^-/- mice. SMTC significantly decreased E_NO by ~30%, but did not change AR in NOS-2^-/- mice. SnPP reduced E_CO in C57Bl6 and IL-10^-/- mice, and increased AR in NOS-2^-/- mice. E_NO decreased as a function of age in IL-10^-/- mice, remaining unchanged in C57Bl6 mice.

Conclusion

These results are consistent with the ideas that: 1) E_NO is associated with mouse strain and knockout differences in NO production and AR, 2) alterations of E_NO and E_CO can be measured non-invasively with induction of allergic AI or inhibition of key gas-producing enzymes, and 3) alterations in AR may be dependent on the relative balance of NO and CO in the airway.     

Biomarkers in osteoarthritis

Biomarkers aid the study of osteoarthritis (OA) in a number of different ways. In this article we summarise briefly their multiple uses and reflect on how the study reported in a previous edition of Arthritis Research & Therapy should promote further investigation of cartilage oligomeric matrix protein (COMP). COMP is foremost among hitherto investigated biomarkers and is most consistently shown to predict knee OA progression. Precisely what role it plays in OA pathogenesis remains unclear and elucidating this may be key to defining, and then targeting, the cellular pathways involved in OA.     

DETECTING DESERTIFICATION PROCESSES USING TM AND ETM+ DATA, NORTH OF ISFAHAN, IRAN

 Aims Desertification results in ecological and biological diminution of the earth, and can happen naturally or cause by anthropogenic activities. This process especially affects arid and semi-arid regions, such as the Isfahan region, where the spread of desertification is reaching critical proportions. The aim of this study is to use remotely sensed data to review the trend of desertification in the northern of Isfahan, Iran. Methods Multi-temporal images were employed to evaluate the trend of desertification, specifically the TM and ETM+ data of September, 1990 and September, 2001. Geometric and radiometric corrections were applied to each image prior to image processing and supervised classification, and vegetation indices were applied to produce a land use map of each image in nine classes. The land use classification s in the two map images were compared and changes between land use classes were detected over the 11 year period using a fuzzy and post-classification technique. Important findings The maps and their comparison with false color composite images showed the differences efficiently. With the fuzzy and post-classification method the land use changes were sited on the map. Fuzzy confirmed 53% changed area and 47% unchanged areas in the study region. The results verify the desertification expansion in the study areas. Because of poor land management, agricultural lands converted to desert and abandoned areas, and some marginal pasture lands had to be changed to agricultural land which are desertification spreading according to United Nations Conference on Desertification (UNCOD). Also farmland and pastures have been converted to urban and industrial areas, and the rangelands have been spoiled due to opencast mine excavations. With the mine margins eroding as well as their debris accumulating on the pasture lands, desertification has become worse. Three areas of less-elevated mountains have remained unchanged. This study confirmed that the anthropogenic activities accelerated the desertification process and severely endangered the remaining areas.     

Blood glutathione and cysteine concentrations in twin children

Glutathione and cysteine are major antioxidants in blood that are associated with health and longevity. To ensure their measurement, careful attention to avoid auto-oxidation is necessary to stabilize the samples. Since no report of these compounds has been reported in children, our goal was to determine their levels of reduced and oxidized glutathione (GSH and GSSG) and cysteine (Cys and CSSC), To this end, 140 healthy children, ages 2 to 9 years from the Louisville Twin Study were studied. Blood samples were collected and analyzed for GSH, GSSG, Cys, and CSSC by our HPLC dual electrochemical method. The results showed that GSH and total GSH (GSH + GSSG) levels for monozygotic (MZ) twins were significantly higher (P < 0.001) than levels for dizygotic (DZ) twins. However, the opposite occurred for Cys and total Cys (Cys + CSSC) in that the levels were significantly higher for DZ twins than for MZ twins. (P < 0.005-0.013). In spite of this marked difference in zygosity, the within-pair correlations for twin pairs used for estimating heritability suggested that there was a major environmental influence for total GSH and total Cys. Finally. GSH levels were significantly lower for young (2-9 years) children than adults (P < 0.001).     

Frequent occurrence of recognition Site-like sequences in the restriction endonucleases

Background  

There are two different theories about the development of the genetic code. Woese suggested that it was developed in connection with the amino acid repertoire, while Crick argued that any connection between codons and amino acids is only the result of an "accident". This question is fundamental to understand the nature of specific protein-nucleic acid interactions.     

Binding to serine 65‐phosphorylated ubiquitin primes Parkin for optimal PINK1‐dependent phosphorylation and activation

Mutations in the mitochondrial protein kinase PINK1 are associated with autosomal recessive Parkinson disease (PD). We and other groups have reported that PINK1 activates Parkin E3 ligase activity both directly via phosphorylation of Parkin serine 65 (Ser⁶⁵)—which lies within its ubiquitin‐like domain (Ubl)—and indirectly through phosphorylation of ubiquitin at Ser⁶⁵. How Ser⁶⁵‐phosphorylated ubiquitin (ubiquitin^{Phospho‐Ser65}) contributes to Parkin activation is currently unknown. Here, we demonstrate that ubiquitin^{Phospho‐Ser65} binding to Parkin dramatically increases the rate and stoichiometry of Parkin phosphorylation at Ser⁶⁵ by PINK1 in vitro. Analysis of the Parkin structure, corroborated by site‐directed mutagenesis, shows that the conserved His302 and Lys151 residues play a critical role in binding of ubiquitin^{Phospho‐Ser65}, thereby promoting Parkin Ser⁶⁵ phosphorylation and activation of its E3 ligase activity in vitro. Mutation of His302 markedly inhibits Parkin Ser⁶⁵ phosphorylation at the mitochondria, which is associated with a marked reduction in its E3 ligase activity following mitochondrial depolarisation. We show that the binding of ubiquitin^{Phospho‐Ser65} to Parkin disrupts the interaction between the Ubl domain and C‐terminal region, thereby increasing the accessibility of Parkin Ser⁶⁵. Finally, purified Parkin maximally phosphorylated at Ser⁶⁵ in vitro cannot be further activated by the addition of ubiquitin^{Phospho‐Ser65}. Our results thus suggest that a major role of ubiquitin^{Phospho‐Ser65} is to promote PINK1‐mediated phosphorylation of Parkin at Ser⁶⁵, leading to maximal activation of Parkin E3 ligase activity. His302 and Lys151 are likely to line a phospho‐Ser⁶⁵‐binding pocket on the surface of Parkin that is critical for the ubiquitin^{Phospho‐Ser65} interaction. This study provides new mechanistic insights into Parkin activation by ubiquitin^{Phospho‐Ser65}, which could aid in the development of Parkin activators that mimic the effect of ubiquitin^{Phospho‐Ser65}.     

<Emphasis Type="Italic">Cleistocybe</Emphasis>, a new genus of Agaricales

A new clitocyboid genus of Agaricales, Cleistocybe, is described to accommodate the isolated evolutionary position of the new species Cleistocybe vernalis inferred by a previously published multigene phylogenetic study. Cleistocybe is distinguished from other clitocyboid lineages by a combination of morphological characters, including lamellae that become gray in age, an interwoven hymenophoral trama with divergent elements when young, strongly interwoven pileipellis with pigmented and encrusted hyphae, white spore deposit, a distinct or ephemeral fibrillose to submembranous partial veil, and smooth, inamyloid basidiospores that are inequilateral in profile view. Cleistocybe encompasses two species, C. vernalis and Clitocybe gomphidioides, based on morphological comparisons with C. vernalis. Clitocybe subvelosa is confirmed as conspecific with C. gomphidioides based on morphological and ITS sequence comparisons of type collections. Cleistocybe is known only from western North America in coniferous forests and appears most closely related to the ectomycorrhizal genus Catathelasma and the saprotrophic genera Callistosporium, Macrocybe, and Pleurocollybia based on nLSU-rDNA phylogenetic analysis. Together these lineages constitute the Catathelasma clade.     

Effects of PI3K catalytic subunit and Akt isoform deficiency on mTOR and p70S6K activation in myoblasts

The PI3K/Akt/mTOR signaling pathway is critical for cellular growth and survival in skeletal muscle, and is activated in response to growth factors such as insulin-like growth factor-I (IGF-I). We found that in C2C12 myoblasts, deficiency of PI3K p110 catalytic subunits or Akt isoforms had distinct effects on phosphorylation of mTOR and p70S6K. siRNA-mediated knockdown of PI3K p110α, p110β, and simultaneous knockdown of p110α and p110β resulted in increased basal and IGF-I-stimulated phosphorylation of mTOR S2448 and p70S6K T389; however, phosphorylation of S6 was reduced in p110β-deficient cells, possibly due to reductions in total S6 protein. We found that IGF-I-stimulated Akt1 activity was enhanced in Akt2- or Akt3-deficient cells, and that knockdown of individual Akt isoforms increased mTOR/p70S6K activation in an isoform-specific fashion. Conversely, levels of IGF-I-stimulated p70S6K phosphorylation in cells simultaneously deficient in both Akt1 and Akt3 were increased beyond those seen with loss of any single Akt isoform, suggesting an alternate, Akt-independent mechanism that activates mTOR/p70S6K. Our results collectively suggest that mTOR/p70S6K is activated in a PI3K/Akt-dependent manner, but that in the absence of p110α or Akt, alternate pathway(s) may mediate activation of mTOR/p70S6K in C2C12 myoblasts.