As the data volume continues to grow exponentially, there is an increasing demand for large storage system capacity. Data compression techniques effectively reduce the volume of written data, enhancing space efficiency. As a result, many modern SSDs have already incorporated data compression capabilities. However, data compression introduces additional processing overhead in critical I/O paths, potentially affecting system performance. Currently, most compression solutions in flash-based storage systems employ fixed compression algorithms for all incoming data without leveraging differences among various data access patterns. This leads to sub-optimal compression efficiency. This article proposes a data-type-aware Flash Translation Layer (DAFTL) scheme to maximize space efficiency without compromising system performance. First, we propose an I/O behavior prediction method to forecast future access on specific data. Then, DAFTL matches data types with distinct I/O behaviors to compression algorithms of varying intensities, achieving an optimal balance between performance and space efficiency. Specifically, it employs higher-intensity compression algorithms for less frequently accessed data to maximize space efficiency. For frequently accessed data, it utilizes lower-intensity but faster compression algorithms to maintain system performance. Finally, an improved compact compression method is proposed to effectively eliminate page fragmentation and further enhance space efficiency. Extensive evaluations using a variety of real-world workloads, as well as the workloads with real data we collected on our platforms, demonstrate that DAFTL achieves more data reductions than other approaches. When compared to the state-of-the-art compression schemes, DAFTL reduces the total number of pages written to the SSD by an average of 8%, 21.3%, and 25.6% for data with high, medium, and low compressibility, respectively. In the case of workloads with real data, DAFTL achieves an average reduction of 10.4% in the total number of pages written to SSD. Furthermore, DAFTL exhibits comparable or even improved read and write performance compared to other solutions.

3D QLC NAND flash memories are now widely applied in storage systems due to their high density. They adopt the two-step programming strategy to avoid severe program interference. This strategy results in a non-trivial time period between the two programming steps, during which the data could be invalidated from update operations. The second programming step might be performed on invalid data, which is defined as invalid programming in this work. We investigate the severity of the invalid programming issue by presenting the elapsed time between the two steps and the ratio of pages that suffer from invalid programming. By varying several parameters of the evaluated storage system, we present that the issue is common in 3D QLC-based storage systems. Finally, we introduce two pilot solutions to deal with the issue in our future work.

The cell cycle of Caulobacter crescentus involves the polar morphogenesis and an asymmetric cell division driven by precise interactions and regulations of proteins, which makes Caulobacter an ideal model organism for investigating bacterial cell development and differentiation. The abundance of molecular data accumulated on Caulobacter motivates system biologists to analyze the complex regulatory network of cell cycle via quantitative modeling. In this paper, We propose a comprehensive model to accurately characterize the underlying mechanisms of cell cycle regulation based on the study of: a) chromosome replication and methylation; b) interactive pathways of five master regulatory proteins including DnaA, GcrA, CcrM, CtrA, and SciP, as well as novel consideration of their corresponding mRNAs; c) cell cycle-dependent proteolysis of CtrA through hierarchical protease complexes. The temporal dynamics of our simulation results are able to closely replicate an extensive set of experimental observations and capture the main phenotype of seven mutant strains of Caulobacter crescentus. Collectively, the proposed model can be used to predict phenotypes of other mutant cases, especially for nonviable strains which are hard to cultivate and observe. Moreover, the module of cyclic proteolysis is an efficient tool to study the metabolism of proteins with similar mechanisms.

Circadian rhythms in a wide range of organisms are mediated by molecular mechanisms based on transcription-translation feedback. In this paper, we use bifurcation theory to explore mathematical models of genetic oscillators, based on Kim & Forger's interpretation of the circadian clock in mammals. At the core of their models is a negative feedback loop whereby PER proteins (PER1 and PER2) bind to and inhibit their transcriptional activator, BMAL1. For oscillations to occur, the dissociation constant of the PER:BMAL1 complex, [Formula: see text], must be ≤ 0.04 nM, which is orders of magnitude smaller than a reasonable expectation of 1-10 nM for this protein complex. We relax this constraint by two modifications to Kim & Forger's 'single negative feedback' (SNF) model: first, by introducing a multistep reaction chain for posttranscriptional modifications of Per mRNA and posttranslational phosphorylations of PER, and second, by replacing the first-order rate law for degradation of PER in the nucleus by a Michaelis-Menten rate law. These modifications increase the maximum allowable [Formula: see text] to ~2 nM. In a third modification, we consider an alternative rate law for gene transcription to resolve an unrealistically large rate of Per2 transcription at very low concentrations of BMAL1. Additionally, we studied extensions of the SNF model to include a second negative feedback loop (involving REV-ERB) and a supplementary positive feedback loop (involving ROR). Contrary to Kim & Forger's observations of these extended models, we find that, with our modifications, the supplementary positive feedback loop makes the oscillations more robust than observed in the models with one or two negative feedback loops. However, all three models are similarly robust when accounting for circadian rhythms (~24 h period) with [Formula: see text] ≥ 1 nM. Our results provide testable predictions for future experimental studies.

[This corrects the article DOI: 10.1371/journal.pcbi.1007842.].

The mammalian circadian clock is deeply rooted in rhythmic regulation of gene expression. Rhythmic transcriptional control mediated by the circadian transcription factors is thought to be the main driver of mammalian circadian gene expression. However, mounting evidence has demonstrated the importance of rhythmic post-transcriptional controls, and it remains unclear how the transcriptional and post-transcriptional mechanisms collectively control rhythmic gene expression. In mouse liver, hundreds of genes were found to exhibit rhythmicity in poly(A) tail length, and the poly(A) rhythms are strongly correlated with the protein expression rhythms. To understand the role of rhythmic poly(A) regulation in circadian gene expression, we constructed a parsimonious model that depicts rhythmic control imposed upon basic mRNA expression and poly(A) regulation processes, including transcription, deadenylation, polyadenylation, and degradation. The model results reveal the rhythmicity in deadenylation as the strongest contributor to the rhythmicity in poly(A) tail length and the rhythmicity in the abundance of the mRNA subpopulation with long poly(A) tails (a rough proxy for mRNA translatability). In line with this finding, the model further shows that the experimentally observed distinct peak phases in the expression of deadenylases, regardless of other rhythmic controls, can robustly cluster the rhythmic mRNAs by their peak phases in poly(A) tail length and abundance of the long-tailed subpopulation. This provides a potential mechanism to synchronize the phases of target gene expression regulated by the same deadenylases. Our findings highlight the critical role of rhythmic deadenylation in regulating poly(A) rhythms and circadian gene expression.