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Person reidentification (Re-ID) aims at recognizing the same identity across different camera views. However, the cross resolution of images [high resolution (HR) and low resolution (LR)] is unavoidable in a realistic scenario due to the various distances among cameras and pedestrians of interest, thus leading to cross-resolution person Re-ID problems. Recently, most cross-resolution person Re-ID methods focus on solving the resolution mismatch problem, while the distribution mismatch between HR and LR images is another factor that significantly impacts the person Re-ID performance. In this article, we propose a dually distribution pulling network (DDPN) to tackle the distribution mismatch problem. DDPN is composed of two modules, that is: 1) super-resolution module and 2) person Re-ID module. They attempt to pull the distribution of LR images closer to the distribution of HR images from image and feature aspects, respectively, through optimizing the maximum mean discrepancy losses. Extensive experiments have been conducted on three benchmark datasets and the results demonstrate the effectiveness of DDPN. Remarkably, DDPN shows a great advantage when compared to the state-of-the-art methods, for instance, we achieve rank-1 accuracy of 76.9% on VR-Market1501, which outperforms the best existing cross-resolution person Re-ID method by 10%.

Burkholderia cenocepacia is an opportunistic pathogen that causes severe infections of the cystic fibrosis (CF) lung. To acquire iron, B. cenocepacia secretes the Fe(III)-binding compound, ornibactin. Genes for synthesis and utilisation of ornibactin are served by the iron starvation (IS) extracytoplasmic function (ECF) σ factor, OrbS. Transcription of orbS is regulated in response to the prevailing iron concentration by the ferric uptake regulator (Fur), such that orbS expression is repressed under iron-sufficient conditions. Here we show that, in addition to Fur-mediated regulation of orbS, the OrbS protein itself responds to intracellular iron availability. Substitution of cysteine residues in the C-terminal region of OrbS diminished the ability to respond to Fe(II) in vivo. Accordingly, whilst Fe(II) impaired transcription from and recognition of OrbS-dependent promoters in vitro by inhibiting the binding of OrbS to core RNA polymerase (RNAP), the cysteine-substituted OrbS variant was less responsive to Fe(II). Thus, the cysteine residues within the C-terminal region of OrbS contribute to an iron-sensing motif that serves as an on-board ‘anti-σ factor’ in the presence of Fe(II). A model to account for the presence two regulators (Fur and OrbS) that respond to the same intracellular Fe(II) signal to control ornibactin synthesis and utilisation is discussed.

Person re-identification (re-ID) is a technique aiming to recognize person cross different cameras. Although some supervised methods have achieved favorable performance, they are far from practical application owing to the lack of labeled data. Thus, unsupervised person re-ID methods are in urgent need. Generally, the commonly used approach in existing unsupervised methods is to first utilize the source image dataset for generating a model in supervised manner, and then transfer the source image domain to the target image domain. However, images may lose their identity information after translation, and the distributions between different domains are far away. To solve these problems, we propose an image domain-to-domain translation method by keeping pedestrian's identity information and pulling closer the domains' distributions for unsupervised person re-ID tasks. Our work exploits the CycleGAN to transfer the existing labeled image domain to the unlabeled image domain. Specially, a Self-labeled Triplet Net is proposed to maintain the pedestrian identity information, and maximum mean discrepancy is introduced to pull the domain distribution closer. Extensive experiments have been conducted and the results demonstrate that the proposed method performs superiorly than the state-ofthe- art unsupervised methods on DukeMTMC-reID and Market- 1501.

OrbS and PvdS are extracytoplasmic function (ECF) σ factors that regulate transcription of operons required for the biosynthesis of the siderophores ornibactin and pyoverdine in the Burkholderia cepacia complex and Pseudomonas spp., respectively. Here we show that promoter recognition by OrbS requires specific tetrameric −35 and −10 element sequences that are strikingly similar to those of the consensus PvdS-dependent promoter. However, whereas Pseudomonas aeruginosa PvdS can serve OrbS-dependent promoters, OrbS cannot utilize PvdS-dependent promoters. To identify features present at OrbS-dependent promoters that facilitate recognition by OrbS, we carried out a detailed analysis of the nucleotide sequence requirements for promoter recognition by both OrbS and PvdS. This revealed that DNA sequence features located outside the sigma binding elements are required for efficient promoter utilization by OrbS. In particular, the presence of an A-tract extending downstream from the −35 element at OrbS-dependent promoters was shown to be an important contributor to OrbS specificity. Our observations demonstrate that the nature of the spacer sequence can have a major impact on promoter recognition by some ECF σ factors through modulation of the local DNA architecture. IMPORTANCE ECF σ factors regulate subsets of bacterial genes in response to environmental stress signals by directing RNA polymerase to promoter sequences known as the −35 and −10 elements. In this work, we identify the −10 and −35 elements that are recognized by the ECF σ factor OrbS. Furthermore, we demonstrate that efficient promoter utilization by this σ factor also requires a polyadenine tract located downstream of the −35 region. We propose that the unique architecture of A-tract DNA imposes conformational features on the −35 element that facilitates efficient recognition by OrbS. Our results show that sequences located between the core promoter elements can make major contributions to promoter recognition by some ECF σ factors.

Upon starvation for glucose or any other core nutrient, yeast cells exit from the mitotic cell cycle and acquire a set of G0-specific characteristics to ensure long-term survival. It is not well understood whether or how cell cycle progression is coordinated with the acquisition of different G0-related features during the transition to stationary phase (SP). Here, we identify the yeast GSK-3 homologue Mck1 as a key regulator of G0 entry and reveal that Mck1 acts in parallel to Rim15 to activate starvation-induced gene expression, the acquisition of stress resistance, the accumulation of storage carbohydrates, the ability of early SP cells to exit from quiescence, and their chronological lifespan. FACS and microscopy imaging analyses indicate that Mck1 promotes mother-daughter cell separation and together with Rim15, modulates cell size. This indicates that the two kinases coordinate the transition-phase cell cycle, cell size and the acquisition of different G0-specific features. Epistasis experiments place MCK1, like RIM15, downstream of RAS2 in antagonising cell growth and activating stress resistance and glycogen accumulation. Remarkably, in the ras2∆ cells, deletion of MCK1 and RIM15 together, compared to removal of either of them alone, compromises respiratory growth and enhances heat tolerance and glycogen accumulation. Our data indicate that the nutrient sensor Ras2 may prevent the acquisition of G0-specific features via at least two pathways. One involves the negative regulation of the effectors of G0 entry such as Mck1 and Rim15, while the other likely to involve its functions in promoting respiratory growth, a phenotype also contributed by Mck1 and Rim15., Author Summary The vast majority of eukaryotic cells exist in a non-proliferating state known as G0. However, how cells transit into, and survive during, the G0 state is poorly understood. Dysregulation of the G0 state leads to age-related diseases such as Alzheimer’s or cancers. We have revealed that the yeast Mck1 and Rim15 kinases, which function downstream of the PKA and/or TOR signaling pathways, coordinate cell cycle progression, cell size homeostasis, and the acquisition of a variety of G0-specific characteristics during the transition into stationary phase. Failure of this coordination compromises the ability of early stationary-phase cells to exit from quiescence and severely shortens their chronological lifespan. Further genetic analyses suggest that the nutrient sensor Ras2 may antagonize G0 entry via at least two pathways, one through the negative regulation of the G0-specific effectors (Mck1 and Rim15) and the other possibly involving its functions in promoting respiratory growth, a phenotype also intricately modulated by Mck1 and Rim15. As Ras2 and Rim15 have homolog in both insects and/or mammals, the identification of the GSK-3 homologue Mck1 and the characterisation of its relationship with Rim15 and Ras2 in G0 entry could provide important clues to the regulation of these processes in more complex organisms.