By Theodore Friedmann, Jay C. Dunlap, Stephen F. Goodwin
The booklet constantly publishes very important reports of the broadest curiosity to geneticists and their colleagues in affiliated disciplines, seriously interpreting destiny directions.
1. Genetics and Pharmacology of sturdiness: the line to Therapeutics for fit Aging
Jorge Iv?n Castillo-Quan, Kerri J. Kinghorn and Ivana Bjedov
2. MicroRNAs: instruments of Mechanistic Insights and organic Therapeutics Discovery for the infrequent Neurogenetic Syndrome Lesch-Nyhan illness (LND)
3. Small RNAs in micro organism and Archaea: Who they're, What They Do, and the way They Do It
E. Gerhart H. Wagner and Pascale Romby
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Additional resources for Advances in Genetics
Hence, it is not surprising that extensive research has identiﬁed aberrant mRNA regulation in neurodegeneration and aging (Abe & Bonini, 2012; Szafranski, Abraham, & Mekhail, 2015). The ﬁrst discovered miRNA, lin-4, regulates longevity and its canonical target is lin-14. Studies in C. elegans showed that either a loss of function lin-4 mutant or a gain of function lin-14 mutant shortened life span, while overexpression mutants showed life span extension (Boehm & Slack, 2005). , 2012). In higher organisms, correlations between miRNA expression and aging are being documented at a tissue-speciﬁc level, but experimental evidence of the direct regulation of life span and healthspan is still unclear (Emde & Hornstein, 2014).
2011). , 2014). , 2011). , 2010; Tullet, 2014). It has been documented that the DAF-16 transcriptional response includes the activation of cellular defense mechanisms, including genes with antioxidant properties like superoxide dismutases and catalases (ﬁve and three, respectively in C. elegans), genes encoding for peptides with antipathogenicity effects, detoxiﬁcation, and heat-shock proteins (Murphy, 2006; Shore & Ruvkun, 2013). 2 mTORC1 Regulation of Longevity Interlinked with the IIS pathway is the mechanistic target of rapamycin (mTOR).
2014). Caenorhabditis elegans with reduced AAK-2, the worm homolog of the a subunit of human AMPK, have reduced life span, while worms with higher expression of aak-2 live 13% longer than controls (Apfeld, O’Connor, McDonagh, DiStefano, & Curtis, 2004). , 2011). , 2007). In Drosophila, ubiquitous down-regulation of the a catalytic subunit of AMPK leads to pre-pupal death. Furthermore, tissuespeciﬁc knockdown in muscle, the fat body or neurons allows normal development, but shortens life span when the knockdown occurs during development and adulthood.
Advances in Genetics by Theodore Friedmann, Jay C. Dunlap, Stephen F. Goodwin