PER1 and PER2 are phosphorylated by CK1ε, which leads to increased ubiquitylation and degradation. The phase of PER1 mRNA expression varies between tissues, The transcript leaves the nucleus and is translated into a protein with PAS domains, which enable protein-protein interactions. Heterodimer CLOCK- BMAL1 activates E-box elements present in the PER1 promoter, as well activating the E box promoters of other components of the molecular clock such as PER2, CRY1, and CRY2. PER1 transcription is regulated by protein interactions with its five E-box and one D-box elements in its promoter region. The PER1 mRNA is expressed in all cells, acting as a part of a transcription-translation negative feedback mechanism, which creates a cell autonomous molecular clock. This light exposure causes increases in PER1 mRNA, suggesting that the PER1 gene plays an important role in entrainment of the mammalian biological clock to the light-dark cycle. Phase shifts in PER1 neurons can be induced by a strong, brief light stimulus to the SCN of rats. In addition, mice with knockouts in both the PER1 and PER2 genes show no circadian rhythmicity. For example, PER1 knockouts affect food entrainable oscillators and methamphetamine-sensitive circadian oscillators, whose periods are altered in the absence of PER1. PER1 is involved in generating circadian rhythms in the SCN, and also has an effect on other oscillations throughout the body. This rhythm is sustained in constant darkness, and can also be entrained to changing light cycles. PER1 is rhythmically transcribed in the SCN, keeping a period of approximately 24 hours. The PER1 gene, also called rigui, is a characteristic circadian oscillator. Thus mPer1 and mPer2 can function as clock components in flies and may have implications concerning the homology of per genes. They found that both mPer constructs could restore rhythm to arrhythmic flies (per01 flies). In this study, mouse mPer1 and mPer2 genes were driven by Drosophila timeless promoter in Drosophila melanogaster. įunctional conservation of the PER gene is shown in a study by Shigeyoshi et al. Still, some believe that even silent mutations can cause significant behavioral phenotypes, and result in major phase changes. Many scientists state that there are no known polymorphisms of the human PER1 gene with significance at a population level that results in measurable behavioral or physiological changes. There is some disagreement between experts over the occurrence of polymorphisms with functional significance. Alternative splicing has been observed in this gene however, these variants have not been fully described. The time of gene expression is sensitive to light, as light during a mammal's subjective night results in a sudden increase in per expression and thus a shift in phase in the suprachiasmatic nucleus. Subsequently, a shift in the light/dark cycle evokes a proportional shift of gene expression in the suprachiasmatic nucleus. Circadian expression of PER1 in the suprachiasmatic nucleus will free-run in constant darkness, meaning that the 24-hour period of the cycle will persist without the aid of external light cues. Genes in this family encode components of the circadian rhythms of locomotor activity, metabolism, and behavior. PER1 is also expressed throughout mammalian peripheral tissues. PER1 is most notably expressed in the region of the brain called the suprachiasmatic nucleus (SCN), which is the primary circadian pacemaker in the mammalian brain. It is expressed with a daily oscillating circadian rhythm, or an oscillation that cycles with a period of approximately 24 hours. This gene is a member of the period family of genes. The PER1 protein is important to the maintenance of circadian rhythms in cells, and may also play a role in the development of cancer. The PER1 gene encodes the period circadian protein homolog 1 protein in humans. positive regulation of transcription by RNA polymerase II.entrainment of circadian clock by photoperiod.negative regulation of transcription, DNA-templated.posttranscriptional regulation of gene expression.circadian regulation of gene expression.negative regulation of I-kappaB kinase/NF-kappaB signaling.negative regulation of transcription by RNA polymerase II.regulation of cytokine production involved in inflammatory response.
regulation of transcription, DNA-templated.negative regulation of glucocorticoid receptor signaling pathway.
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