The moment magnitude () 5.4 Pohang earthquake, the most damaging event in South Korea since instrumental seismic observation began in 1905, occurred beneath the Pohang geothermal power plant in 2017. Geological and geophysical data suggest that the Pohang earthquake was induced by fluid from an enhanced geothermal system (EGS) site, which was injected directly into a near-critically stressed subsurface fault zone. The magnitude of the mainshock makes it the largest known induced earthquake at an EGS site.

The substantial importance of P-selectin glycoprotein ligand 1 (PSGL-1) in leukocyte trafficking has continued to emerge beyond its initial identification as a selectin ligand. PSGL-1 seemed to be a relatively simple molecule with an extracellular mucin domain extended as a flexible rod, teleologically consistent with its primary role in tethering leukocytes to endothelial selectins. The rolling interaction between leukocyte and endothelium mediated by this selectin-PSGL-1 interaction requires branched O-glycan extensions on specific PSGL-1 amino acid residues. In some cells, such as neutrophils, the glycosyltransferases involved in formation of the O-glycans are constitutively expressed, while in other cells, such as T cells, they are expressed only after appropriate activation. Thus, PSGL-1 supports leukocyte recruitment in both innate and adaptive arms of the immune response. A complex array of amino acids within the selectins engage multiple sugar residues of the branched O-glycans on PSGL-1 and provide the molecular interactions responsible for the velcro-like catch bonds that support leukocyte rolling. Such binding of PSGL-1 can also induce signaling events that influence cell phenotype and function. Scrutiny of PSGL-1 has revealed a better understanding of how it performs as a selectin ligand and yielded unexpected insights that extend its scope from supporting leukocyte rolling in inflammatory settings to homeostasis including stem cell homing to the thymus and mature T-cell homing to secondary lymphoid organs. PSGL-1 has been found to bind homeostatic chemokines CCL19 and CCL21 and to support the chemotactic response to these chemokines. Surprisingly, the O-glycan modifications of PSGL-1 that support rolling mediated by selectins in inflammatory conditions interfere with PSGL-1 binding to homeostatic chemokines and thereby limit responsiveness to the chemotactic cues used in steady state T-cell traffic. The multi-level influence of PSGL-1 on cell traffic in both inflammatory and steady state settings is therefore substantially determined by the orchestrated addition of O-glycans. However, central as specific O-glycosylation is to PSGL-1 function, in vivo regulation of PSGL-1 glycosylation in T cells remains poorly understood. It is our purpose herein to review what is known, and not known, of PSGL-1 glycosylation and to update understanding of PSGL-1 functional scope.

CD34 is a cell-surface sialomucin expressed by hematopoietic stem cells (HSC), mast cells, and vascular endothelia. Despite its popularity as an HSC marker, the function of CD34 on hematopoietic cells remains enigmatic. Here, we have addressed this issue by examining the behavior of mutant mast cells lacking CD34, the related sialomucin, CD43, or both molecules. Loss of these molecules leads to a gene-dose-dependent increase in mast cell homotypic aggregation with CD34/CD43KOs > CD43KO > CD34KO > wild-type. Importantly, reexpression of CD34 or CD43 in these cells caused reversal of this phenotype. Furthermore, we find that loss of these sialomucins prevents mast cell repopulation and hematopoietic precursor reconstitution in vivo. Our data provide clear-cut evidence for a hematopoietic function for CD34 and suggest that it acts as a negative regulator of cell adhesion.

T cell receptor (TCR) signaling by MHC class I and II induces thymocytes to acquire cytotoxic and helper fates via the induction of Runx3 and ThPOK transcription factors, respectively. The mechanisms by which TCR signaling is translated into transcriptional programs for each cell fate remain elusive. Here, we show that, in post-selection thymocytes, a genome organizer, SATB1, activates genes for lineage-specifying factors, including ThPOK, Runx3, CD4, CD8, and Treg factor Foxp3, via regulating enhancers in these genes in a locus-specific manner. Indeed, SATB1-deficient thymocytes are partially re-directed into inappropriate T lineages after both MHC class I- and II-mediated selection, and they fail to generate NKT and Treg subsets. Despite its essential role in activating enhancers for the gene encoding ThPOK in TCR-signaled thymocytes, SATB1 becomes dispensable for maintaining ThPOK in CD4 T cells. Collectively, our findings demonstrate that SATB1 shapes the primary T cell pool by directing lineage-specific transcriptional programs in the thymus.

Mobile DNAs use many mechanisms to minimize damage to their hosts. Here we show that a subclass of group II introns avoids host damage by inserting directly after transcriptional terminator motifs in bacterial genomes (stem-loops followed by Ts). This property contrasts with the site-specific behavior of most group II introns, which insert into homing site sequences. Reconstituted ribonucleoprotein particles of the Bacillus halodurans intron B.h.I1 are shown to reverse-splice into DNA targets in vitro but require the DNA to be single-stranded and fold into a stem-loop analogous to the RNA structure that forms during transcription termination. Recognition of this DNA stem-loop motif accounts for in vivo target specificity. Insertion after terminators is a previously unrecognized strategy for a selfish DNA because it prevents interruption of coding sequences and restricts expression of the mobile DNA after integration.reverse transcriptase ͉ ribozyme ͉ mobile DNA ͉ bacteria R eduction of host damage is a basic principle of survival for selfish DNAs. The most common mechanisms involve suppression of transcription and translation, and integration into comparatively innocuous sites (1-4). Among retroelements, for example, R2 elements insert site-specifically into defined sequences within rDNA arrays while leaving most rDNAs intact (5). LINE1 elements have a less stringent preference for the sequence TTTTA, which results in integrations into gene-poor regions (6). Other retroelements target genomic loci through protein-protein interactions, to insert at pol III promoters (7), into telomeric elements (8), or into heterochromatin regions (9).Group II intron retroelements avoid host damage in two ways. First, the introns splice out of interrupted sequence at the RNA level to reconstitute functional coding sequence. Second, the introns insert site-specifically into compatible targets through retrohoming, thereby limiting potential targets. The mechanism of retrohoming is well characterized and is carried out by a ribonucleoprotein (RNP) complex composed of excised intron lariat and intron-encoded protein (IEP). The process is initiated by reverse splicing of lariat RNA into the top strand of a DNA target. The bottom strand is cleaved by the endonuclease domain of the IEP, and the integrated intron is reverse transcribed by the IEP, using the cleaved DNA as a primer. Repair processes complete the insertion steps (10-12).Normally, retrohoming of group II introns is highly sitespecific because of an Ϸ20-to 35-bp target sequence. Thirteen positions of the DNA target are recognized by base pairings between the intron RNA and the DNA exons via the interactions IBS1-EBS1, IBS2-EBS2 (intron and exon binding sites 1 and 2; 6 bp each), and either ␦-␦Ј (IIA introns; 1 bp) or IBS3-EBS3 (IIB, IIC introns; 1 bp). Additional target-specificity comes from IEP recognition of upstream exon DNA sequences Ϫ23 to Ϫ1 and downstream exon sequences ϩ4 to ϩ9 (11,13,14).In contrast to such site-specificity, introns of the phylogenetic subclass ''b...