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Potassium (K+) transporters, particularly high-affinity K+ transporters (HKT), are crucial for plant growth and abiotic stress response. These transporters regulate Na+ and K+ balance in the cells to prevent sodium toxicity in plant tissues. Although HKT genes have been extensively studied in various crops, there is a deficiency in their characterization and understanding of their role in wheat, particularly regarding their involvement in adaptive response to environmental stresses like salinity. In this study, several bioinformatics tools including web-based platforms and software applications were employed to identify, characterize and localize HKTs genes within the wheat genome. A greenhouse trial was also conducted to investigate the mRNA expression levels of some of the significant salt-responsive genes in wheat seedlings grown under different concentrations of NaCl (0, 200, and 400 mM). Genome-wide analysis, resulted in identification of 35 TaHKTs that are unevenly distributed on ten chromosomes. The majority of these transporters are localized on plasma membrane. Analysis of promoter regions showed that most of the TaHKT genes have abundant cis-elements that involved in hormones and abiotic stress responses. Gene expression analysis indicated a significant upregulation of TaHKT6 and TaSOS1 genes were found in wheat seedlings treated with 400 mM NaCl. Expression levels of TaNHX1, TaNHX2 and TaTVP1 genes were also higher in 200 mM and 400 mM NaCl-treated plants when compared to non-stressed plants. Overall, the results provide further evidence for the role of the TaHKT in wheat's stress response to elevated salt levels and pave the way for further functional research in K+ transporters in plants.

The introduction of noninvasive prenatal testing has resulted in substantial reductions to previously accepted false-positive rates of prenatal screening. Despite this, the possibility of false-positive results remains a challenging consideration in clinical practice, particularly considering the increasing uptake of genome-wide noninvasive prenatal testing, and the subsequent increased proportion of high-risk results attributable to various biological events besides fetal aneuploidy. Confined placental mosaicism, whereby chromosome anomalies exclusively affect the placenta, is perhaps the most widely accepted cause of false-positive noninvasive prenatal testing. There remains, however, a substantial degree of ambiguity in the literature pertaining to the clinical ramifications of confined placental mosaicism and its potential association with placental insufficiency, and consequentially adverse pregnancy outcomes including fetal growth restriction. Other causes of false-positive noninvasive prenatal testing include vanishing twin syndrome, in which the cell-free DNA from a demised aneuploidy-affected twin triggers a high-risk result, technical failures, and maternal origins of abnormal cell-free DNA such as uterine fibroids or unrecognized mosaicisms. Most concerningly, maternal malignancies are also a documented cause of false-positive screening results. In this review, we compile what is currently known about the various causes of false-positive noninvasive prenatal testing., (Copyright © 2023 The Author(s). Published by Elsevier Inc. All rights reserved.)

Insulin is essential in controlling blood glucose levels, and its synthesis and secretion have been well investigated. In contrast, how insulin secretory granules (ISGs) are degraded in pancreatic beta cells remains largely unknown. To clarify the mechanism, we constructed a fluorescent reporter detecting ISG degradation, where EGFP and mCherry are tandemly conjugated to a cytoplasmic region of ZnT8, an ISG membrane-localized protein. Depletion of serum and amino acid stimulated lysosomal ISG degradation detected with the reporter. Next, with MIN6 cells expressing Cas9 and the reporter, we investigated the involvement of conventional Atg5/7-dependent autophagy to show that it is dispensable for the ISG degradation process. Finally, we performed genome-wide screening by enriching the cells lacking the ISG degradation and showed that pathways regulating autophagy are not identified. These results suggest that alternative degradation in lysosomes, instead of conventional autophagy, may be involved in ISG degradation., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:Yuya Nishida reports financial support was provided by Japan Society for the Promotion of Science. Hirotaka Watada reports financial support was provided by Japan Society for the Promotion of Science. Masato Koike reports financial support was provided by Japan Society for the Promotion of Science., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Powdery mildew, caused by Blumeria graminis f. sp. tritici (Bgt), is a destructive disease affecting wheat crops worldwide. Functional genes can be activated in response to Bgt inoculations. Calcineurin B-like protein (CBL) together with CBL-interacting protein kinase (CIPK) forms the CBL-CIPK protein complex that participates in Ca 2+ sensor kinase-related signaling pathways responding to abiotic and biotic stresses. In this study, we performed a genome-wide screening and identified 27 CIPK subfamilies (123 CIPK transcripts, TaCIPKs) including 55 new and 47 updated TaCIPKs in wheat. Phylogenetic analysis revealed that 123 TaCIPKs could be divided into four groups. Segmental duplications and tandem repeats promoted the expansion of the TaCIPK family. Gene function was further evidenced by differences in gene structure, cis-elements, and protein domains. TaCIPK15-4A was cloned in this study. TaCIPK15-4A contained 17 serine, seven tyrosine, and 15 threonine phosphorylation sites and localized in the plasma membrane and cytoplasm. TaCIPK15-4A expression was induced after Bgt inoculation. Virus-induced gene silencing and overexpression experiments indicated that TaCIPK15-4A could play a positive role in wheat disease resistance to Bgt. Overall, these results provide insights into the role of the TaCIPK gene family in wheat resistance and could be beneficial for further research to prevent Bgt infection., Competing Interests: Declaration of competing interest The authors declare no conflict of interest., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Labial grooves in maxillary incisors have been reported in several wild-type rodent species. Previous studies have reported age-dependent labial grooves occur in moderate prevalence in C57BL/6 mice; however, very little is known about the occurrence of such grooves. In the present study, we observed age-dependent groove formation in C57BL/6 mice up to 26 months after birth and found that not only the frequency of the appearance of incisor grooves but also the number of grooves increased in an age-dependent manner. We examined the molecular mechanisms of age-dependent groove formation by performing DNA microarray analysis of the incisors of 12-month-old (12M) and 24-month-old (24M) mice. Amelx, encoding the major enamel matrix protein AMELOGENIN, was identified as a 12M-specific gene. Comparing with wild-type mice, the maxillary incisors of Amelx -/- mutants indicated the increase of the frequency and number of labial grooves. These findings suggested that the Amelx gene impacts the age-dependent appearance of the labial incisor groove in C57BL/6 mice., (Copyright © 2018 Elsevier Inc. All rights reserved.)

To search for novel target(s) of the Ca(2+)-signaling transducer, calmodulin (CaM), we performed a newly developed genome-wide CaM interaction screening of 19,676 GST-fused proteins expressed in human. We identified striated muscle activator of Rho signaling (STARS) as a novel CaM target and characterized its CaM binding ability and found that the Ca(2+)/CaM complex interacted stoichiometrically with the N-terminal region (Ala13-Gln35) of STARS in vitro as well as in living cells. Mutagenesis studies identified Ile20 and Trp33 as the essential hydrophobic residues in CaM anchoring. Furthermore, the CaM binding deficient mutant (Ile20Ala, Trp33Ala) of STARS further enhanced its stimulatory effect on SRF-dependent transcriptional activation. These results suggest a connection between Ca(2+)-signaling via excitation-contraction coupling and the regulation of STARS-mediated gene expression in muscles., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

Background: Gene set or pathway analysis (GPA) can provide a comprehensive mechanistic overview in delineating molecular pathoetiology of human diseases. Existing tools that can handle for GPA on both mutational and gene expressional aspects are limited. This leads to the development of uGPA (unified Gene Pathway Analyzer)., Methods: uGPA package provides a unified solution to knowledge base-driven competitive GPA that can analyze genome-wide screening data derived from multiple platforms (next generation sequencing or microarray) and sample sources (genomic or transcriptomic) on both mutational and gene expressional perspectives. It allows for a quick assessment of perspective outline of gene sets on the studied disease through enrichment test modeled by cumulative hypergeometric distribution and reports the gene components detected with events (mutation or differential gene expression) in the gene sets., Results: uGPA package has been successfully verified to be applicable on input data generated from NGS-based platforms (transcriptome sequencing and whole-exome sequencing). Genome-wide screening data from other platforms should also apply., Conclusions: uGPA package delivers a simple, flexible and platform-independent functionality to multiple aspects of GPA. It equips clinicians and scientists with a useful tool in studying molecular mechanism of human diseases using modern high-throughput genome-wide screening strategy, which assists personalized therapy., (Copyright © 2015. Published by Elsevier B.V.)