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Piwi protein Miwi is shown to be a small RNA-guided RNase in mice; disrupting the catalytic activity of Miwi results in increased accumulation of LINE1 retrotransposon transcripts and male infertility. Transposon silencing by Piwi proteins The combination of Piwi proteins and their associated Piwi-interacting RNAs (piRNAs) mediates epigenetic transposon silencing in animal germlines. Piwi proteins are predicted to be endonucleases, but the significance of this activity had not been demonstrated in vivo. The laboratories of Dónal O'Carroll and Ramesh Pillai have now made mouse models in which residues expected to be critical for nuclease activity in the three mouse Piwi homologues, Mili, Miwi and Miwi2, are mutated. The mutant mice show phenotypic differences. The Mili and Miwi mutants are defective in piRNA production, transposon silencing and fertility, whereas the Miwi2 mutant has normal piRNA levels, seems to undergo piRNA amplification and silences transposons. These studies highlight distinctions between the murine enzymes responsible for piRNA biogenesis. Repetitive-element-derived Piwi-interacting RNAs (piRNAs).sup.1,2 act together with Piwi proteins Mili (also known as Piwil2) and Miwi2 (also known as Piwil4) in a genome defence mechanism that initiates transposon silencing via DNA methylation in the mouse male embryonic germ line. This silencing depends on the participation of the Piwi proteins in a slicer-dependent piRNA amplification pathway and is essential for male fertility.sup.3,4. A third Piwi family member, Miwi (also known as Piwil1), is expressed in specific postnatal germ cells and associates with a unique set of piRNAs of unknown function.sup.5,6,7. Here we show that Miwi is a small RNA-guided RNase (slicer) that requires extensive complementarity for target cleavage in vitro. Disruption of its catalytic activity in mice by a single point mutation causes male infertility, and mutant germ cells show increased accumulation of LINE1 retrotransposon transcripts. We provide evidence for Miwi slicer activity directly cleaving transposon messenger RNAs, offering an explanation for the continued maintenance of repeat-derived piRNAs long after transposon silencing is established in germline stem cells. Furthermore, our study supports a slicer-dependent silencing mechanism that functions without piRNA amplification. Thus, Piwi proteins seem to act in a two-pronged mammalian transposon silencing strategy: one promotes transcriptional repression in the embryo, the other reinforces silencing at the post-transcriptional level after birth., Author(s): Michael Reuter [sup.1] [sup.2] , Philipp Berninger [sup.1] [sup.2] , Shinichiro Chuma [sup.3] [sup.4] , Hardik Shah [sup.5] , Mihoko Hosokawa [sup.3] [sup.4] , Charlotta Funaya [sup.6] , Claude [...]

A low probability of intercept (LPI), or low probability of detection (LPD) communication technique known as cyclic code shift keying (CCSK) is described. We discuss the basic concepts of CCSK and describe a system based on the use of random or pseudorandom codes for biphase modulation. We use simulation to show that the bit error rate (BER) for CCSK can be closely estimated by using existing equations that apply to M-ary orthogonal signaling (MOS). Also, we show that significantly fewer computations are required for CCSK than for MOS when the number of bits per symbol is the same. We show that using biphase modulation results in waveforms that have a large time-bandwidth product and very low input signal-to-noise ratio (SNR) and thus inherently have an LPI by a radiometer. We evaluate detection by a radiometer and show that LPI can be achieved by using codes of lengths greater than about [2.sup.12] (i.e., by transmitting more than about 12 bits per symbol). Results illustrate the effect that the CCSK symbol length and error probability, and the radiometer integration time and probability of false alarm (PFA), have on detection by a radiometer. We describe a variation of CCSK called truncated CCSK (TCCSK). In this system, the code of length [2.sup.k] is cyclically shifted, then truncated and transmitted. Although shortened, the truncated code still represents k bits of information, thus leading to an increased data rate. We evaluate radiometer detection of TCCSK and it is shown that the probability of detection is increased compared with the detection of CCSK.

We present an approximate analysis approach to the computation of probability of error and mean burst error length for a decision feedback equalizer (DFE) that takes into account feedback of decision errors. The method uses a reduced-state Markov model of the feedback process and is applicable to linear modulation formats. We use this technique to analyze a DFE design that mitigates the effects of feedback error by incorporating a soft decision device into the feedback path and a norm constraint on the feedback filter weights. We apply the DFE design and analysis approach to a dispersive multipath propagation environment. Index Terms--Decision feedback equalizers, error analysis, error propagation, Markov processes.

We propose a numerically efficient technique for calculating the probability of symbol error for arbitrary coherent modulation schemes in the presence of intersymbol interference (ISI) and additive noise. The probability of error is formulated in terms of an inverse Fourier transform of the windowed characteristic function of the random variable representing the interfering symbols and the noise process. The integral is evaluated numerically using the sampling theorem. Index Terms - Intersymbol interference, probability of error.