The rotation rate of a planet is a fundamental parameter, no less than its mass or composition, and planetary investigators require this rate to assess various other phenomena such as planetary wind speeds, internal and atmospheric models, ring dynamics and so forth. Saturn presents a conundrum, however, because none of its various planetary periods indicates the “true” rotation of the planet. Thus, although the planet displays an abundance of periodicities near 10.7 hours, the exact rotation period of Saturn is unknown. In the magnetosphere, “planetary-period oscillations” (PPOs) appear in charged particles, magnetic fields, energetic neutral atoms, radio emissions and motions of the plasma sheet and magnetopause. In Saturn’s rings, the spoke phenomenon can exhibit periodicities near 10.7 hours, and ring phenomena themselves may be related to the interior rotation of the planet. In the high-latitude ionosphere, modulations near this period appear in auroral motions and intensities. In the upper atmosphere, some cloud features rotate near this period, although wind speeds are generally faster, and the well-known polar hexagon rotates with a period close to 10.7 hours. Some of the magnetospheric/ionospheric oscillations differ in the northern and southern hemispheres and their periods do not remain constant, sometimes varying on long time scales of a year or longer and sometimes on much shorter time scales. These variations in the period argue against a cause related to changes interior to Saturn, and because the magnetic and spin axes of Saturn are reported to be axisymmetric (unlike those of any other known planet), Saturn’s periodicities cannot be explained as “wobble” caused by a geometric tilt or by a nondipolar magnetic anomaly. Several models have been proposed to account for the observed periodicities, including rotating atmospheric vortices, periodic plasma releases and a flapping magnetodisk, but none can satisfactorily explain all of Saturn’s periodicities nor their common origin, and none can determine the exact rotation rate of the planet. This chapter reviews Saturn’s periodicities, theories thereof, and how they might be used to determine the elusive rotation rate of the planet.
MicroRNAs (miRNAs) are small, single-stranded RNAs of about 22 nucleotides involved in gene regulation by binding to 3′ untranslated regions (UTRs) of messenger RNAs (mRNAs) (Bartel, 2004). By bringing the RNA-induced silencing complex (RISC) to the mRNAs, they enable gene expression inhibition (gene silencing), either by affecting protein translation or by destabilizing mRNAs through deadenylation or decapping (Fabian et al., 2010). Target mRNAs are recognized by miRNAs through Watson–Crick matching between the nucleotides two to seven of the 5′ end of miRNAs (seed sequences), and complementary sequences called seed sites in the 3′ UTR of mRNAs (Bartel, 2009). Gene silencing by miRNAs is an important mechanism in physiological processes, and its deregulation can lead to complex diseases such as cancer (Garzon et al., 2006).
Complex diseases that are heritable are commonly analysed by studying genomic DNA variants, such as single nucleotide polymorphisms (SNPs), which are a change of one nucleotide that occurs in more than 1% in a population (Frazer et al., 2009). A SNP can take several forms called alleles. Because recombination events between closely located SNPs are less likely than recombination between SNPs that are located far apart on a chromosome, alleles at close SNPs often co-occur, or correlate, in which case the SNPs are said to be in linkage disequilibrium (LD; Reich et al., 2001; Clague et al., 2010).
SNPs in the coding sequence of mRNAs have been well studied for their role in changing the amino-acid chain, as it may result in protein isoforms with affected function, leading to phenotypic differences and also disease. Nevertheless, SNPs can also occur in non-coding regions of the genome such as the 3′ UTR of mRNAs, which harbors many functional sequence elements involved in gene regulation. One type of functional element that can be disrupted by SNPs is the miRNA target site. SNPs in miRNA target sites (miRSNPs) can change the affinity between the miRNA seed sequence and its target mRNA, resulting in deregulation of gene expression (Figure 10.1), and possibly in phenotype differences and diseases (Sethupathy and Collins, 2008).
One classic example that a miRSNP determines phenotype is the single nucleotide change in the myostatin gene (GDF8) of Texel sheep (Clop et al., 2006).
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