Psychoneuroimmunology and Genetics

Psychoneuroimmunology is a study that investigates the interaction between human emotions and the immune system, which is mediated by the endocrine and nervous systems. The nervous and immune systems maintain extensive communication, including communication to lymphoid organs from deep-rooted sympathetic and parasympathetic nerves. Genetic factors are responsible for individual variation in emotional reactivity, and neuroendocrine stress responses were shown by earlier studies in humans. Several gene-environment studies have shown that long-term effects of stress are being moderated by genetic variations in the hypothalamic-pituitary-adrenal (HPA) axis. There is a large interindividual variability of HPA axis stress reactivity on variants of the glucocorticoid (GR) or mineralocorticoid receptor genes, and it documents a sex-specific association between different GR gene polymorphisms and salivary cortisol responses to acute psychosocial stress. In conclusion, many kinds of mind-body behavioral interventions are effective in improving mood, quality of life, reducing stress, and anxiety, thereby altering neuroendocrine and immune functions, and ultimately altering the genetic aberrations. However, the question remains as to whether these latter effects are sufficiently large or last long enough to contribute to health benefits, or if they are even relevant to the development of a disease

Telomere Maintenance in Organisms without Telomerase

Biochemistr

Chapter Telomere Maintenance in Organisms without Telomerase

Biochemistr

Protein Interactions on Telomeric Retrotransposons in Drosophila

Telomere length in Drosophila is maintained by targeted transposition of three non-LTR retrotransposons: HeT-A, TART and TAHRE (HTT), but understanding the regulation of this process is hindered by our poor knowledge of HTT associated proteins. We have identified new protein components of the HTT array: Chromator (Chro), the TRF2/DREF complex and the sumoylation machinery. Chro was localized on telomeric HTT arrays by immunostaining, where it may interact with Prod directly, as indicated by yeast two-hybrid interaction, co-IP, and colocalization on polytene chromosomes. The TRF2/DREF complex may promote the open structure of HTT chromatin. The protein interactions controlling HTT chromatin structure and telomere length may be modulated by sumoylation

Protein Interactions on Telomeric Retrotransposons in Drosophila

Telomere length in Drosophila is maintained by targeted transposition of three non-LTR retrotransposons: HeT-A, TART and TAHRE (HTT), but understanding the regulation of this process is hindered by our poor knowledge of HTT associated proteins. We have identified new protein components of the HTT array: Chromator (Chro), the TRF2/DREF complex and the sumoylation machinery. Chro was localized on telomeric HTT arrays by immunostaining, where it may interact with Prod directly, as indicated by yeast two-hybrid interaction, co-IP, and colocalization on polytene chromosomes. The TRF2/DREF complex may promote the open structure of HTT chromatin. The protein interactions controlling HTT chromatin structure and telomere length may be modulated by sumoylation

Identification of the <i>Telomere elongation</i> mutation in <i>Drosophila</i>

Background. Telomeres in Drosophila melanogaster are similar to those of other eukaryotes in terms of their function, although they are formed by non-LTR retrotransposons instead of telomerase-based short repeats. The length of the telomeres in Drosophila depends on the number of copies of these transposable elements. A dominant mutation, Tel1, causes a several-fold elongation of telomeres. Methods. In this study we identified the Tel1 mutation by a combination of transposon-induced, site-specific recombination and next generation sequencing. Results. Recombination located Tel1 to a 15 kb region in 92A. Comparison of the DNA sequence in this region with the Drosophila Genetic Reference Panel of wild type genomic sequences delimited Tel1 to a 3 bp deletion inside intron 8 of Ino80. Discussion. The mapped Tel1 mutation (3-bp deletion found in Ino80) did not appear to affect the quantity or length of the Ino80 transcript. Tel1 causes a significant reduction in transcripts of CG18493, a gene nested in an intron 8 of Ino80, which is expressed in ovaries and expected to encode a serine-type peptidase.</jats:p