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A low-power and area optimized 28-nm CMOS 28-Gb/s transceiver is presented. The transceiver comprised with one PLL shared with 4 transceiver lanes. To meet the CEI-28G-VSR and CAUI4 (chip-to-module) standards, a 1-tap DFE is employed for the receiver. The power reduction is realized by employing 1-tap loop unrolled DFE circuits with domino logic and dynamic latches, and eliminating FFE. The transceiver occupies 2.31 mm2 and consumes 505 mW (4.5 pJ/bit).

A high bandwidth and a robust performance are demanded in the consumer market applications. An ADC-based transceiver satisfies these demands and enables power/area scaling with process [1,2]. We developed and tested a spread-spectrum-clocking (SSC) compliant 5-Gb/s transceiver in 65-nm CMOS. The receiver uses an ADC-based front-end that samples the incoming signal without adjusting the phase relation between the sampling clock and the signal, hence eliminating the need for phase control of the sampling clock (Fig. 8.7.1). The phase tracking of the incoming signal and the data decision are performed entirely in the numerical domain without generating physical sampling-clock phases. An adaptive digital FFE (feed-forward equalizer) compensates for a channel loss up to 15dB at 2.5 GHz, using an on-chip adaptation controller based on CMA (constant-modulus algorithm). The CDR operated with BER less than 1E-12 when the transmitter and receiver clock signals were independently SSC-modulated at a modulation frequency of 30 kHz with a frequency deviation of 0 to −5000ppm.

The thymus is a vertebrate-specific organ where T lymphocytes are generated. Genetic programs that lead to thymus development are incompletely understood. We previously screened ethylnitrosourea-induced medaka mutants for recessive defects in thymus development. Here we report that one of those mutants is caused by a missense mutation in a gene encoding the previously uncharacterized protein WDR55 carrying the tryptophan-aspartate-repeat motif. We find that WDR55 is a novel nucleolar protein involved in the production of ribosomal RNA (rRNA). Defects in WDR55 cause aberrant accumulation of rRNA intermediates and cell cycle arrest. A mutation in WDR55 in zebrafish also leads to analogous defects in thymus development, whereas WDR55-null mice are lethal before implantation. These results indicate that WDR55 is a nuclear modulator of rRNA synthesis, cell cycle progression, and embryonic organogenesis including teleost thymus development., Author Summary Medaka, Oryzias latipes, is a small freshwater fish that is useful for studies of forward and reverse genetics. The availability of various inbred strains is the distinct advantage of medaka over zebrafish, especially in studies of the immune system. The thymus is a primary immune organ that is unique to vertebrates and supports the generation of T lymphocytes. Defective thymus development tends to cause abnormal T lymphocyte development, resulting in immunodeficiency or autoimmunity. However, the molecular pathways underlying thymus development have not been fully uncovered. Here we report the positional cloning of a gene responsible for one of the thymus-defective medaka mutants. We find that the hkc phenotype is caused by a missense mutation in a gene encoding the previously uncharacterized protein WDR55. Our results indicate that WDR55 is a novel nucleolar modulator of rRNA biosynthesis, cell cycle progression, and vertebrate development of organs, including teleost thymus. These results not only provide evidence of the existence of a new mechanism of rRNA production but also demonstrate that the malfunction of WDR55 causes cell cycle arrest and developmental failure, including defective thymus development.