Novel SLC30A2 mutations in the pathogenesis of transient neonatal zinc deficiency.

Importance: Transient neonatal zinc deficiency (TNZD) occurs in breastfed infants due to abnormally low breast milk zinc levels. Mutations in the solute carrier family 30 member 2 (SLC30A2) gene, which encodes the zinc transporter ZNT2, cause low zinc concentration in breast milk. Objective: This study aimed to provide further insights into TNZD pathophysiology. Methods: SLC30A2 sequencing was performed in three unrelated Japanese mothers, whose infants developed TNZD due to low-zinc milk consumption. The effects of the identified mutations were examined using cell-based assays and luciferase reporter analysis. Results: Novel SLC30A2 mutations were identified in each mother. One harbored a heterozygous missense mutation in the ZNT2 zinc-binding site, which resulted in defective zinc transport. The other two mothers exhibited multiple heterozygous mutations in the SLC30A2 promoter, the first mutations in the SLC30A2 regulatory region reported to date. Interpretation: This report provides new genetic insights into TNZD pathogenesis in breastfed infants.

E-cadherin-dependent coordinated epithelial rotation on a two-dimensional discoidal pattern.

In vivo, cells collectively migrate in a variety of developmental and pathological contexts. Coordinated epithelial rotation represents a unique type of collective cell migrations, which has been modeled in vitro under spatially confined conditions. Although it is known that the coordinated rotation depends on intercellular interactions, the contribution of E-cadherin, a major cell-cell adhesion molecule, has not been directly addressed on two-dimensional (2D) confined substrates. Here, using well-controlled fibronectin-coated surfaces, we tracked and compared the migratory behaviors of MDCK cells expressing or lacking E-cadherin. We observed that wild-type MDCK II cells exhibited persistent and coordinated rotations on discoidal patterns, while E-cadherin knockout cells migrated in a less coordinated manner without large-scale rotation. Our comparison of the collective dynamics between these two cell types revealed a series of changes in migratory behavior caused by the loss of E-cadherin, including a decreased global migration speed, less regularity in quantified coordination, and increased average density of topological defects. Taken together, these data demonstrate that spontaneous initiation of collective epithelial rotations depends on E-cadherin under 2D discoidal confinements.

Pararhizobium mangrovi sp. nov., Isolated From Aegiceras corniculatum Stem.

A novel Gram-stain-negative, catalase- and oxidase-positive, motile, short rod-shaped bacterium designated BGMRC 6574T was isolated from stems of Aegiceras corniculatum collected from Hainan province, China. The strain grew at 25-37 °C (optimal at 28 °C), pH 5.0-10.0 (pH 7.0), and 3-8% (w/v) NaCl (3%). Based on the 16S rRNA phylogenetic analysis, the strain was closely related to Pararhizobium haloflavum MCCC 1K03228T (96.45% sequence similarity). The novel strain showed an average nucleotide identity value and a digital DNA-DNA hybridization of 72.62 and 27.1%, respectively, to P. haloflavum MCCC 1K03228T based on draft genome sequences. The G+C content of the genomic DNA was 64.7 mol%. The major respiratory quinone was Q-10. The strain possessed genes putatively encoding choline uptake and conversion to betaine gene clusters. The extract significantly delayed the lifespan of Caenorhabditis elegans compared to the control (P < 0.05). The major polar lipids were phosphatidylcholine, seven unidentified phospholipids, three unidentified ninhydrin-positive phospholipids, and two unidentified lipids. The major cellular fatty acid was C19:0 cyclo ω8c. The results of a polyphasic taxonomic study showed that strain BGMRC 6574T represents a new species of the genus Pararhizobium, and it was named Pararhizobium mangrovi sp. nov. The type strain is BGMRC 6574T (=KCTC 72636T = CGMCC 1.16783).