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FCS-like zinc finger (FLZ) proteins are plant-specific regulatory proteins, which contain a highly conserved FLZ domain, and they play critical roles in plant growth and stress responses. Although the FLZ family has been systematically characterized in certain plants, it remains underexplored in Brassica species, which are vital sources of vegetables, edible oils, and condiments for human consumption and are highly sensitive to various abiotic stresses. Following the whole-genome triplication events (WGT) in Brassica, elucidating how the FLZ genes have expanded, differentiated, and responded to abiotic stresses is valuable for uncovering the genetic basis and functionality of these genes. In this study, we identified a total of 113 FLZ genes from three diploid Brassica species and classified them into four groups on the basis of their amino acid sequences. Additionally, we identified 109 collinear gene pairs across these Brassica species, which are dispersed among different chromosomes, suggesting that whole-genome duplication (WGD) has significantly contributed to the expansion of the FLZ family. Subcellular localization revealed that six representative BolFLZ proteins are located in the nucleus and cytoplasm. Yeast two-hybrid assays revealed that 13 selected BolFLZs interact with BolSnRK1α1 and BolSnRK1α2, confirming the conservation of the SnRK1α-FLZ module in Brassica species. Expression profile analysis revealed differential expression patterns of BolFLZ across various tissues. Notably, the expression levels of seven BolFLZ genes out of the fifteen genes analyzed changed significantly following treatment with various abiotic stressors, indicating that the BolFLZ genes play distinct physiological roles and respond uniquely to abiotic stresses in Brassica species. Together, our results provide a comprehensive overview of the FLZ gene family in Brassica species and insights into their potential applications for enhancing stress tolerance and growth in Chinese kale. [ABSTRACT FROM AUTHOR]

The purpose of crowd counting is to estimate the number of pedestrians in crowd images. Crowd counting or density estimation is an extremely challenging task in computer vision, due to large scale variations and dense scene. Current methods solve these issues by compounding multi-scale Convolutional Neural Network with different receptive fields. In this paper, a novel end-to-end architecture based on Multi-Scale Adversarial Convolutional Neural Network (MSA-CNN) is proposed to generate crowd density and estimate the amount of crowd. Firstly, a multi-scale network is used to extract the globally relevant features in the crowd image, and then fractionally-strided convolutional layers are designed for up-sampling the output to recover the loss of crucial details caused by the earlier max pooling layers. An adversarial loss is directly employed to shrink the estimated value into the realistic subspace to reduce the blurring effect of density estimation. Joint training is performed in an end-to-end fashion using a combination of Adversarial loss and Euclidean loss. The two losses are integrated via a joint training scheme to improve density estimation performance.We conduct some extensive experiments on available datasets to show the significant improvements and supremacy of the proposed approach over the available state-of-the-art approaches.

The purpose of crowd counting is to estimate the number of pedestrians in crowd images. Crowd counting or density estimation is an extremely challenging task in computer vision, due to large scale variations and dense scene. Current methods solve these issues by compounding multi-scale Convolutional Neural Network with different receptive fields. In this paper, a novel end-to-end architecture based on Multi-Scale Adversarial Convolutional Neural Network (MSA-CNN) is proposed to generate crowd density and estimate the amount of crowd. Firstly, a multi-scale network is used to extract the globally relevant features in the crowd image, and then fractionally-strided convolutional layers are designed for up-sampling the output to recover the loss of crucial details caused by the earlier max pooling layers. An adversarial loss is directly employed to shrink the estimated value into the realistic subspace to reduce the blurring effect of density estimation. Joint training is performed in an end-to-end fashion using a combination of Adversarial loss and Euclidean loss. The two losses are integrated via a joint training scheme to improve density estimation performance.We conduct some extensive experiments on available datasets to show the significant improvements and supremacy of the proposed approach over the available state-of-the-art approaches. [ABSTRACT FROM AUTHOR]

Preeclampsia is a cardiovascular disorder of late pregnancy that is, commonly characterized by hypertension, renal structural damage and dysfunction, and fetal growth restriction. Prevailing etiologic models of this disorder include T-cell dysfunction as an initiating cause of preeclampsia. Indoleamine 2,3-dioxygenase ( IDO), an enzyme that mediates the conversion of tryptophan to kynurenine, has been linked to preeclampsia in humans, and is known to regulate T-cell activity and an endothelial-derived relaxing factor. To test the hypothesis that IDO is causally involved in the pathogenesis of preeclampsia, mice deficient for IDO ( IDO- KO) were generated on a C57 BL/6 background. IDO- KO and wild-type C57 BL/6 mice were bred, and preeclampsia phenotypes were evaluated during pregnancy. Pregnant IDO- KO mice exhibited pathognomonic renal glomerular endotheliosis, proteinuria, pregnancy-specific endothelial dysfunction, intrauterine growth restriction, and mildly elevated blood pressure compared to wild-type mice. Together these findings highlight an important role for IDO in the generation of phenotypes typical of preeclampsia. Loss of IDO function may represent a risk factor for the development of preeclampsia. By extension, increased IDO activity, reductions in IDO reactants, or increases in IDO products may represent novel therapeutic approaches for this disorder. [ABSTRACT FROM AUTHOR]

Background: DNA variation in Interferon Regulatory Factor 6 ( IRF6) contributes risk for orofacial clefting, including a common DNA variant rs642961. This DNA variant is located in a multi-species conserved sequence that is 9.7 kb upstream from the IRF6 transcriptional start site ( MCS9.7). The MCS9.7 element was shown to possess enhancer activity that mimicked the expression of endogenous Irf6 at embryonic day 11.5 in transient transgenic embryos, and also contains a p63 binding site that transactivates IRF6 expression. To analyze whether the MCS9.7 enhancer is sufficient to drive IRF6 expression, we generated stable transgenic murine lines that carry a MCS9.7-lacZ transgene. We hypothesized that MCS9.7 was sufficient to recapitulate the endogenous expression of Irf6 at other time-points during embryonic development. Results: We observed that MCS9.7 activity recapitulated endogenous Irf6 expression in most tissues, but not in the medial edge epithelium (MEE) at E14.5, when Irf6 expression was high during secondary palatal fusion. Also, while MCS9.7 activity and Irf6 expression were associated with p63 expression, we observed MCS9.7 activity and Irf6 expression in periderm, although p63 was absent. Conclusion: These data suggest that MCS9.7 enhancer activity is not sufficient to recapitulate IRF6 expression, and that p63 expression is not always necessary nor sufficient for transactivation of IRF6. Developmental Dynamics 241:340-349, 2012. © 2011 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Summary: The iron exporter ferroportin (Fpn) is essential to transfer iron from cells to plasma. Systemic iron homeostasis in vertebrates is regulated by the hepcidin-mediated internalization of Fpn. Here, we demonstrate a second route for Fpn internalization; when cytosolic iron levels are low, Fpn is internalized in a hepcidin-independent manner dependent upon the E3 ubiquitin ligase Nedd4-2 and the Nedd4-2 binding protein Nfdip-1. Retention of cell-surface Fpn through reductions in Nedd4-2 results in cell death through depletion of cytosolic iron. Nedd4-2 is also required for internalization of Fpn in the absence of ferroxidase activity as well as for the entry of hepcidin-induced Fpn into the multivesicular body. C. elegans lacks hepcidin genes, and C. elegans Fpn expressed in mammalian cells is not internalized by hepcidin but is internalized in response to iron deprivation in a Nedd4-2-dependent manner, supporting the hypothesis that Nedd4-2-induced internalization of Fpn is evolutionarily conserved. [ABSTRACT FROM AUTHOR]

We report a mouse model of multiple osteochondromas (MO), an autosomal dominant disease in humans, also known as multiple hereditary exostoses (MHE or HME) and characterized by the formation of cartilage-capped osseous growths projecting from the metaphyses of endochondral bones. The pathogenesis of these osteochondromas has remained unclear. Mice heterozygous for Exti or Ext2, modeling the human genotypes that cause MO, occasionally develop solitary osteochondroma-like structures on ribs [Lin et al. (2000) Dev Biol 224(2):299-311; Stickens et al. (2005) Development 132(22):5055-5068]. Rather than model the germ-line genotype, we modeled the chimeric tissue genotype of somatic loss of heterozygosity (LOH). by conditionally inactivating Ext1 via headto-head loxP sites and temporally controlled Cre-recombinase in chondrocytes. These mice faithfully recapitulate the human phenotype of multiple metaphyseal osteochondromas. We also confirm homozygous disruption of Exti in osteochondroma chondrocytes and their origin in proliferating physeal chondrocytes. These results explain prior modeling failures with the necessity for somatic LOH in a developmentally regulated cell type. [ABSTRACT FROM AUTHOR]

The primary product of the renin gene is preprorenin. A signal peptide sorts renin to the secretory pathway in juxtaglomerular cells where it is released into the circulation to initiate the renin-angiotensin system cascade. In the brain, transcription of renin occurs from an alternative promoter encoding an mRNA starting with a new first exon (exon 1b). Exon 1b initiating transcripts skip over the classical first exon (exon 1a) containing the initiation codon for preprorenin. Exon 1b transcripts are predicted to use a highly conserved initiation codon within exon 2, producing renin, which should remain intracellular, because it lacks the signal peptide. To evaluate the roles of secreted and intracellular renin, we took advantage of the organization of the renin locus to generate a secreted renin (sRen)-specific knockout, which preserves intracellular renin expression. Expression of sRen mRNA was ablated in the brain and kidney, whereas intracellular renin mRNA expression was preserved in fetal and adult brains. We noted a developmental shift from the expression of sRen mRNA in the fetal brain to intracellular renin mRNA in the adult brain. Homozygous sRen knockout mice exhibited very poor survival at weaning. The survivors exhibited renal lesions, low hematocrit, an inability to generate a concentrated urine, decreased arterial pressure, and impaired aortic contraction. These results suggest that preservation of intracellular renin expression in the brain is not sufficient to compensate for a loss of sRen, and sRen plays a pivotal role in renal development and function, survival, and the regulation of arterial pressure. [ABSTRACT FROM AUTHOR]