Weak signal detection technique based on Durbin-Watson test and one-bit sampling.

Correlation-based detection techniques are widely used in the weak periodic signal detection field. Traditionally, they are based on extracting the correlation of a weak signal from noise. Considering the impact of a weak signal on the randomness of background noise, this article takes the opposite approach and proposes a weak signal detection technique based on the Durbin-Watson (DW) test and one-bit sampling, detecting the weak signal due to the extent to which the randomness of noise is affected. The randomness of noise is analyzed through the DW test, which is a method for detecting the randomness of data sequences through first-order autocorrelation. One-bit sampling is adopted to reduce the complexity of the sampling circuit and data processing algorithm. The effectiveness of the DW test in the situation of one-bit sampling is demonstrated through simulation and analysis. Simulation results show that the proposed technique is capable of detecting weak sinusoidal and square-wave signals with a signal-to-noise ratio (SNR) above -30 dB, and the frequency or SNR of a weak signal can be further estimated based on mutual constraints. The measured results confirm the capability. In addition, the factors of coherent sampling, noise bandwidth, and comparator threshold that influence the performance of the proposed technique are simulated and discussed in detail.

QSER1 preserves the suppressive status of the pro-apoptotic genes to prevent apoptosis.

Activation of the pro-apoptotic genes by the p53 family is a critical step in induction of apoptosis. However, the molecular signaling underlying their suppression remains largely unknown. Here, we report a general role of QSER1 in preventing apoptosis. QSER1 is widely up-regulated in multiple cancers, and its up-regulation correlates with poor clinic outcomes. QSER1 knockdown significantly promotes apoptosis in both p53 wild type and mutant cancer cells. Interestingly, we show that QSER1 and p53 occupy distinct cis-regulatory regions in a common subset of the pro-apoptotic genes, and function antagonistically to maintain their proper expression. Furthermore, we identify a key regulatory DNA element named QSER1 binding site in PUMA (QBP). Deletion of QBP de-represses PUMA and induces apoptosis. Mechanistically, QSER1 functions together with SIN3A to suppress PUMA in a p53-dependent and -independent manner, suggesting that QSER1 inhibition might be a potential therapeutic strategy to induce apoptosis in cancers.

ZFP281-BRCA2 prevents R-loop accumulation during DNA replication.

R-loops are prevalent in mammalian genomes and involved in many fundamental cellular processes. Depletion of BRCA2 leads to aberrant R-loop accumulation, contributing to genome instability. Here, we show that ZFP281 cooperates with BRCA2 in preventing R-loop accumulation to facilitate DNA replication in embryonic stem cells. ZFP281 depletion reduces PCNA levels on chromatin and impairs DNA replication. Mechanistically, we demonstrate that ZFP281 can interact with BRCA2, and that BRCA2 is enriched at G/C-rich promoters and requires both ZFP281 and PRC2 for its proper recruitment to the bivalent chromatin at the genome-wide scale. Furthermore, depletion of ZFP281 or BRCA2 leads to accumulation of R-loops over the bivalent regions, and compromises activation of the developmental genes by retinoic acid during stem cell differentiation. In summary, our results reveal that ZFP281 recruits BRCA2 to the bivalent chromatin regions to ensure proper progression of DNA replication through preventing persistent R-loops.