Empirical evidence of the mediterranean fruit fly movement between orchard types

Understanding species movement in the agroecological system is an important theme in ecology. A mark–release–capture experiment was conducted to study the dispersion behaviour of the Mediterranean fruit fly, Ceratitis capitata (Wied.; Diptera: Tephritidae; Medfly) in northern Israel. Four pairs of pear and citrus orchards were selected for the field experiments. Sterile flies dyed with different colours were released in three seasons during 2015 and 2016, based on the phenological stages of the hosts. The total number of captured marked sterile flies per trap (FT) was approx 300 in both April and August. In November, FT values decreased by about 35% to approximately 200. The wild Medfly that were also captured showed an opposite trend, from an FT of 1.8 and 6.4 in April and August, respectively, to an FT of about 330 in November. Marked sterile flies were captured in both the release and the neighbouring orchard sites. We found that the Medfly migrates from pear to citrus orchards during spring and from citrus to pear during summer, when there are no fruit-bearing trees in the orchards. However, during November, when the wild Medfly population prevails in the area, a clear pattern of migration is hard to identify, perhaps because of a possible interaction with the wild fly's population.     

Colicinogeny of O157:H7 enterohemorrhagic Escherichia coli and the shielding of colicin and phage receptors by their O-antigenic side chains.

Twenty O157:H7 enterohemorrhagic Escherichia coli strains from patients with different clinical conditions were tested for colicinogeny and the presence of Verotoxin (VT) genes. From bloody diarrhea cases, 7/8 isolates and from hemolytic uremic syndrome cases 3/5 isolates all synthesized what appeared to be colicin D. The remaining strains, which included 7 from asymptomatic sources, were noncolicinogenic. The plasmid determining the colicin was found to be 1.4 kb larger than the 5.2-kb pColD. The colicin D protein had a molecular weight of about 90,000, whereas the O157 colicin was 87,000. The plasmid was designated pColD157 to reflect these differences. Of O157:H7 isolates 17/20 had genes for both of the Verotoxins VT1 and VT2, and the remaining 3/20 for VT1 only. There was no correlation between the presence of VT determinants and colicinogeny or symptoms. The O157:H7 strains exhibited significant resistance to other colicins and bacteriophages.     

Exposure by males to light emitted from media devices at night is linked with decline of sperm quality and correlated with sleep quality measures

ABSTRACT

The last several decades have been characterized by the widespread usage of digital devices, especially smartphones. At the same time, there have been reports of both decline in sleep duration and quality and male fertility decline. The aim of this study was to assess the relationship between evening exposure to the light-emitting screens of digital media devices and measures of both sleep and sperm quality. Semen samples were obtained from 116 men undergoing fertility evaluation for the following sperm variables: volume (mL), pH, sperm concentration (million/mL), motility percentage (progressive% + non-progressive motility%), and total sperm count. Exposure to the screens of electronic devices and sleep habits was obtained by means of a questionnaire. Smartphone and tablet usage in the evening and after bedtime was negatively correlated with sperm motility (?0.392; ?0.369; p < .05), sperm progressive motility (?0.322; ?0.299; p < .05), and sperm concentration (?0.169; p < .05), and positively correlated with the percentage of immotile sperm (0.382; 0.344; p < .05). In addition, sleep duration was positively correlated with sperm total and progressive motility (0.249; 0.233; p < .05) and negatively correlated with semen pH (?0.349; p < .05). A significant negative correlation was observed between subjective sleepiness and total and progressive motility (?0.264; p < .05) as well as total motile sperm number (?0.173; p < .05). The results of this study support a link between evening and post-bedtime exposure to light-emitting digital media screens and sperm quality. Further research is required to establish the proposed causative link and may lead to the future development of relevant therapeutic and lifestyle interventions.     

Specificity of latent TGF-β binding protein (LTBP) incorporation into matrix: Role of fibrillins and fibronectin

Fibrillin microfibrils are extracellular matrix structures with essential functions in the development and the organization of tissues including blood vessels, bone, limbs and the eye. Fibrillin‐1 and fibrillin‐2 form the core of fibrillin microfibrils, to which multiple proteins associate to form a highly organized structure. Defining the components of this structure and their interactions is crucial to understand the pathobiology of microfibrillopathies associated with mutations in fibrillins and in microfibril‐associated molecules. In this study, we have analyzed both in vitro and in vivo the role of fibrillin microfibrils in the matrix deposition of latent TGF‐β binding protein 1 (LTBP‐1), ‐3 and ‐4; the three LTBPs that form a complex with TGF‐β. In Fbn1^?/? ascending aortas and lungs, LTBP‐3 and LTBP‐4 are not incorporated into a matrix lacking fibrillin‐1 microfibrils, whereas LTBP‐1 is still deposited. In addition, in cultures of Fbn1^?/? smooth muscle cells or lung fibroblasts, LTBP‐3 and LTBP‐4 are not incorporated into a matrix lacking fibrillin‐1 microfibrils, whereas LTBP‐1 is still deposited. Fibrillin‐2 is not involved in the deposition of LTBP‐1 in Fbn1^?/? extracellular matrix as cells deficient for both fibrillin‐1 and fibrillin‐2 still incorporate LTBP‐1 in their matrix. However, blocking the formation of the fibronectin network in Fbn1^?/? cells abrogates the deposition of LTBP‐1. Together, these data indicate that LTBP‐3 and LTBP‐4 association with the matrix depends on fibrillin‐1 microfibrils, whereas LTBP‐1 association depends on a fibronectin network. J. Cell. Physiol. 227: 3828–3836, 2012. © 2012 Wiley Periodicals, Inc.     

TCR zeta down-regulation under chronic inflammation is mediated by myeloid suppressor cells differentially distributed between various lymphatic organs

T cell AgR zeta chain down-regulation associated with T cell dysfunction has been described in cancer, infectious, and autoimmune diseases. We have previously shown that chronic inflammation is mandatory for the induction of an immunosuppressive environment leading to this phenomenon. To identify the key immunosuppressive components, we used an in vivo mouse model exhibiting chronic inflammation-induced immunosuppression. Herein, we demonstrate that: 1) under chronic inflammation secondary lymphatic organs display various immunological milieus; zeta chain down-regulation and T cell dysfunction are induced in the spleen, peripheral blood, and bone marrow, but not in lymph nodes, correlating with elevated levels of Gr1(+)Mac-1(+) myeloid suppressor cells (MSC); 2) MSC are responsible for the induction of such an immunosuppression under both normal and inflammatory conditions; and 3) normal T cells administered into mice exhibiting an immunosuppressive environment down-regulate their zeta expression. Such an environment is anticipated to limit the success of immunotherapeutic strategies based on vaccination and T cell transfer, which are currently under investigation for immunotherapy of cancer.     

Capturing cellular machines by systematic screens of protein complexes

Two recent studies have provided the most complete screen for protein complexes in yeast to date, in which partners were identified for approximately half of the proteome. A comparison shows that these two datasets are complementary. In addition, one of the analyses points to a modular organization of the cellular protein network. These data will prove useful in defining principles and trends that arise when combining large-scale datasets of different natures, and in deriving properties of protein machines in cellular systems.     

A genome-wide screen for essential yeast genes that affect telomere length maintenance

Telomeres are structures composed of repetitive DNA and proteins that protect the chromosomal ends in eukaryotic cells from fusion or degradation, thus contributing to genomic stability. Although telomere length varies between species, in all organisms studied telomere length appears to be controlled by a dynamic equilibrium between elongating mechanisms (mainly addition of repeats by the enzyme telomerase) and nucleases that shorten the telomeric sequences. Two previous studies have analyzed a collection of yeast deletion strains (deleted for nonessential genes) and found over 270 genes that affect telomere length (Telomere Length Maintenance or TLM genes). Here we complete the list of TLM by analyzing a collection of strains carrying hypomorphic alleles of most essential genes (DAmP collection). We identify 87 essential genes that affect telomere length in yeast. These genes interact with the nonessential TLM genes in a significant manner, and provide new insights on the mechanisms involved in telomere length maintenance. The newly identified genes span a variety of cellular processes, including protein degradation, pre-mRNA splicing and DNA replication.