2016 AQ Summit: Education Update by Laurie Bragg

An update on the University of Maine\u27s SEANET educational outreach programs

2016 AQ Summit: Education Update on SEANET by Laurie Bragg

Maine EPSCoR and the Aquaculture Research Institute at the University of Maine received a five year, $20 million grant from the National Science Foundation (NSF) to build the Sustainable Ecological Aquaculture Network (SEANET). This includes developing and building Maine\u27s workforce in sustainable aquaculture. SEANET supports a broad portfolio of workforce development and educational outreach

Practice Matters: Screening and Monitoring Hyperlipidemia

Abstract The purpose of this article is to provide Faith Community Nurses with current information on hyperlipidemia, a chronic disease responsible for the leading cause of death worldwide. Current guidelines for cholesterol screening and a risk calculator resource for estimating cardiovascular risk are provided. Myths and truths are presented for review with patients. Suggestions and resources for lifestyle modifications and patient education are included. Faith Community Nurses are at the center of community health and actively involved with improving health outcomes related to chronic disease

Maine EPSCoR, vol. 1, issue 1

The University of Maine recently gained Carnegie R1 status, a level of recognition that speaks to the quality and scale of research happening at Maine’s land grant, sea grant, and space grant institution, and across the state as a whole. Research institutes, centers and labs established because of NSF EPSCoR RII Track-1 grants have created a significant and lasting impact in Maine. These entities include the Advanced Structures and Composites Center, Frontier Institute for Research in Sensor Technologies, Forest Bioproducts Research Institute, and Mitchell Center for Sustainability Solutions, which have generated over 500 million dollars in new R&D funding for the state following the completion of their RII Track-1 support. Maine EPSCoR’s current NSF EPSCoR RII Track-1 grant, Maine-eDNA, is set to embark on a full field season with work occurring throughout the state. We recognize the researchers, staff, graduate students, and undergraduate students who continue to actively participate in this work. Their effort and resilience in the face of uncertain and changing circumstances is inspiring and makes real contributions in our efforts to expand educational opportunities in STEM, drive workforce development, and strengthen research capacity in the state of Maine

2015 Proceedings: Religious Values

Paving the Way to Global Christian Citizenshiphttps://knowledge.e.southern.edu/reysymp/1003/thumbnail.jp

Mutant allele-specific CRISPR disruption in DYT1 dystonia fibroblasts restores cell function

Most individuals affected with DYT1 dystonia have a heterozygous 3-bp deletion in the TOR1A gene (c.907_909delGAG). The mutation appears to act through a dominant-negative mechanism compromising normal torsinA function, and it is proposed that reducing mutant torsinA may normalize torsinA activity. In this study, we used an engineered Cas9 variant from Streptococcus pyogenes (SpCas9-VRQR) to target the mutation in the TOR1A gene in order to disrupt mutant torsinA in DYT1 patient fibroblasts. Selective targeting of the DYT1 allele was highly efficient with most common non-homologous end joining (NHEJ) edits, leading to a predicted premature stop codon with loss of the torsinA C terminus (delta 302–332 aa). Structural analysis predicted a functionally inactive status of this truncated torsinA due to the loss of residues associated with ATPase activity and binding to LULL1. Immunoblotting showed a reduction of the torsinA protein level in Cas9-edited DYT1 fibroblasts, and a functional assay using HSV infection indicated a phenotypic recovery toward that observed in control fibroblasts. These findings suggest that the selective disruption of the mutant TOR1A allele using CRISPR-Cas9 inactivates mutant torsinA, allowing the remaining wild-type torsinA to exert normal function

Disease onset in X-linked dystonia-parkinsonism correlates with expansion of a hexameric repeat within an SVA retrotransposon in TAF1

X-linked dystonia-parkinsonism (XDP) is a neurodegenerative disease associated with an antisense insertion of a SINE-VNTR-Alu (SVA)-type retrotransposon within an intron of TAF1. This unique insertion coincides with six additional noncoding sequence changes in TAF1, the gene that encodes TATA-binding protein–associated factor-1, which appear to be inherited together as an identical haplotype in all reported cases. Here we examined the sequence of this SVA in XDP patients (n = 140) and detected polymorphic variation in the length of a hexanucleotide repeat domain, (CCCTCT)n. The number of repeats in these cases ranged from 35 to 52 and showed a highly significant inverse correlation with age at disease onset. Because other SVAs exhibit intrinsic promoter activity that depends in part on the hexameric domain, we assayed the transcriptional regulatory effects of varying hexameric lengths found in the unique XDP SVA retrotransposon using luciferase reporter constructs. When inserted sense or antisense to the luciferase reading frame, the XDP variants repressed or enhanced transcription, respectively, to an extent that appeared to vary with length of the hexamer. Further in silico analysis of this SVA sequence revealed multiple motifs predicted to form G-quadruplexes, with the greatest potential detected for the hexameric repeat domain. These data directly link sequence variation within the XDP-specific SVA sequence to phenotypic variability in clinical disease manifestation and provide insight into potential mechanisms by which this intronic retroelement may induce transcriptional interference in TAF1 expression