			Home About us Contact

Models Suggesting (models + suggesting)

Distribution by Scientific Domains

Life Sciences	50%

Selected Abstracts

Cryptic variation in butterfly eyespot development: the importance of sample size in gene expression studies

EVOLUTION AND DEVELOPMENT, Issue 1 2007
Robert D. Reed
SUMMARY Previous studies have shown that development can be robust to variation in parameters such as the timing or level of gene expression. This leads to the prediction that natural populations should be able to host developmental variation that has little phenotypic effect. Cryptic variation is of particular interest because it can result in selectable phenotypes when "released" by environmental or genetic factors. Currently, however, we have little idea of how variation is distributed between genes or over time in pattern formation processes. Here we survey expression of Notch (N), Spalt (Sal), and Engrailed (En) during butterfly eyespot determination to better understand how pattern formation may vary within a population. We observed substantial heterochronic variance in the progress of spatial expression patterns for all three proteins, suggesting some degree of developmental buffering in eyespot development. Peak variance for different proteins was found at both early and late stages of development, contrasting with previous models suggesting that the distribution of variance should be more temporally focused during pattern formation. We speculate that our observations are representative of a standing reservoir of cryptic variation that may contribute to phenotypic evolution under certain circumstances. Our results also provide a strong cautionary message that gene expression studies with limited sample sizes can be positively misleading in terms of inferring expression pattern time series, as well as for making cross-species phylogenetic comparisons. [source]

Relationships Between Attitudes Toward Organizations and Performance Appraisal Systems and Rating Behavior

INTERNATIONAL JOURNAL OF SELECTION AND ASSESSMENT, Issue 3 2001
Aharon Tziner
Data collected in seven separate samples in three countries (the USA, Canada and Israel) were used to examine the relationships between perceptions of one's organization (climate, commitment), beliefs about appraisal systems (self-efficacy, uses of appraisal) and raters' orientations to appraisal systems (confidence and comfort) and specific rating behaviors. We obtained good fits for structural models suggesting that attitudes and beliefs accounted for substantial variance in raters' likelihood of giving high or low ratings, willingness to discriminate good from poor performers, and willingness to discriminate among various aspects of job performance when completing actual performance ratings. Proximal attitudes and beliefs (i.e., those directly related to the performance appraisal system) appear to have stronger links to rating behavior than do more distal attitudes (i.e., attitudes toward the organization in general). [source]

Epigenetic regulation of the non-canonical Wnt pathway in acute myeloid leukemia

CANCER SCIENCE, Issue 2 2010
Vanesa Martín
Wnt5a is a member of the Wnt family of proteins that signals through the non-canonical Wnt/Ca2+pathway to suppress cyclin D1. Deregulation of this pathway has been found in animal models suggesting that it acts as tumour suppressor in acute myeloid leukemia (AML). Although DNA methylation is the main mechanism of regulation of the canonical Wnt pathway in AML, the role of WNT5A abnormalities has never been evaluated in this clinical setting. The methylation status of WNT5A promoter,exon 1 was analyzed by methylation-specific PCR and sequencing in eleven AML-derived cell lines and 252 AML patients. We observed WNT5A hypermethylation in seven cell lines and in 43% (107/252) of AML patients. WNT5A methylation was associated with decreased WNT5A expression (P < 0.001) that was restored after exposure to 5-Aza-2'-deoxycytidine. Moreover, WNT5A hypermethylation correlated with upregulation of CYCLIN D1 expression (P < 0.001). Relapse (15%vs 37%, P < 0.001) and mortality (61%vs 79%, P = 0.004) rates were lower for patients in the non-methylated group. Disease-free survival and overall survival at 6 and 7 years, respectively, were 60% and 27% for unmethylated patients and 20% and 0% for hypermethylated patients (P = 0.0001 and P = 0.04, respectively). Interestingly, significant differences were also observed when the analysis was carried out according to cytogenetic risk groups. We demonstrate that WNT5A, a putative tumor suppressor gene in AML, is silenced by methylation in this disease and that this epigenetic event is associated with upregulation of CYCLIN D1 expression and confers poor prognosis in patients with AML. (Cancer Sci 2009) [source]

Characterization of mediators of microbial virulence and innate immunity using the Caenorhabditis elegans host,pathogen model

CELLULAR MICROBIOLOGY, Issue 7 2003
Rosanna A. Alegado
Summary The soil-borne nematode, Caenorhabditis elegans, is emerging as a versatile model in which to study host,pathogen interactions. The worm model has shown to be particularly effective in elucidating both microbial and animal genes involved in toxin-mediated killing. In addition, recent work on worm infection by a variety of bacterial pathogens has shown that a number of virulence regulatory genes mediate worm susceptibility. Many of these regulatory genes, including the PhoP/Q two-component regulators in Salmonella and LasR in Pseudomonas aeruginosa, have also been implicated in mammalian models suggesting that findings in the worm model will be relevant to other systems. In keeping with this concept, experiments aimed at identifying host innate immunity genes have also implicated pathways that have been suggested to play a role in plants and animals, such as the p38 MAP kinase pathway. Despite rapid forward progress using this model, much work remains to be done including the design of more sensitive methods to find effector molecules and further characterization of the exact interaction between invading pathogens and C. elegans' cellular components. [source]