Suitable plant architecture is a key factor in maximizing crop yield, and stem growth habit is a crucial characteristic of architecture in soybean. Here, we investigated the combined effects of the Dt2 gene, which produces a semi-determinate growth habit, and a loss-of-function e1-nl allele of the floral repressor E1. Comparisons among near-isogenic lines with different maturity genotypes indicated that the loss or repression of E1 function enhanced the effect of Dt2 on main-stem node numbers. Dt2 expression in stem tips was up-regulated in early growth stages under long-day conditions by the Dt2 and e1-nl alleles in an additive manner. Additionally, an Arabidopsis APETALA1 ortholog was highly up-regulated in a Dt2/e1-nl line. EMSAs revealed that the E1 DNA-binding domain bound to several genomic sites harboring key polymorphisms that differentiate Dt2 from dt2 alleles. One of these sites had different transcription activities between the Dt2 and dt2 alleles, and these activities were repressed by E1. Taken together, our results suggest that the Dt2 allele confers semi-determinacy by being preferentially induced when released from the repression by E1. The allelic combination of Dt2 and e1-nl confers a distinct semi-determinate phenotype, which would facilitate the use of the Dt2 allele, particularly under long days at high latitudes.

Compartmentalization of secondary lymphoid organs is orchestrated by specialized fibroblastic reticular cells (FRCs), which guide immune cell migration, interaction, and function. Here, we investigated the pathways driving FRC differentiation into functionally distinct subsets. A Notch signaling signature distinguished lymph node (LN) FRCs, and deletion of Notch1 and Notch2 in FRCs restricted functional specialization, particularly for T-zone FRCs (T-zone reticular cells [TRCs]). Dendritic cell (DC)-specific deletion of the Notch ligand Jagged-1 prevented Ccl19hi TRC differentiation, with homeostatic Ccr7+ DCs also being required for their maintenance. The resulting Ccl19 chemokine expression supported formation of central T-zone sub-compartments enriched in Xcr1+ DCs and CD8+ T cells. Both the spatial organization and Notch2-Jagged1 signaling activity were conserved in human LNs. Disrupting T-zone segregation via Notch2 inactivation in FRCs impaired the generation of CD8+ T cell memory precursors. Thus, Notch2-dependent TRC programming by DCs shapes distinct T-zone niches that sustain CD8+ T cell immunity.

ABSTRACT Invasive populations are predicted to have reduced genetic diversity due to bottleneck events. The parasitoid wasp Melittobia sosui was previously identified only in the subtropical area of the southern Japanese islands and Taiwan but was recently found in the temperate area of the Japanese mainland. The distribution of this species may have recently expanded northward due to factors such as climatic events and global warming. The population genetics of both the native and invasive regions were investigated using mitochondrial and nuclear microsatellite DNA. As expected, mitochondrial variation was observed in the native region but not in the invasive region, which had only one haplotype. However, the two regions exhibited similar levels of microsatellite variation, and an average of 43% and 38% of alleles were uniquely found in the native and invasive populations, respectively. The difference in genetic variation between mitochondrial and microsatellite DNA in the invasive populations may be explained by the faster mutation rate of microsatellites, as well as the population structure of Melittobia, in which the subdivision into small inbreeding lineages may facilitate the accumulation of mutations. The high proportion of private alleles suggests that the mainland population diverged from the native populations at least 100 years ago, ruling out the possibility that the mainland population was established recently. The present study suggests that M. sosui might have already existed on the mainland but at a low frequency or that the mainland population was derived from a ghost population that diverged from the native populations more than 100 years ago.

Modern crops were created through the domestication and genetic introgression of wild relatives and adaptive differentiation in new environments. Identifying the domestication-related genes and unveiling their molecular diversity provide clues for understanding how the domesticated variants were selected by ancient people, elucidating how and where these crops were domesticated. Molecular genetics and genomics have explored some domestication-related genes in soybean ( Glycine max ). Here, we summarize recent studies about the quantitative trait locus (QTL) and genes involved in the domestication traits, introduce the functions of these genes, clarify which alleles of domesticated genes were selected during domestication. A deeper understanding of soybean domestication could help to break the bottleneck of modern breeding by highlighting unused genetic diversity not selected in the original domestication process, as well as highlighting promising new avenues for the identification and research of important agronomic traits among different crop species.

Mobilization of transposable elements (TEs) is suppressed by epigenetic mechanisms involving cytosine methylation. How-ever, few studies have focused on clarifying relationships between epigenetic influences of TEs on the adjacent DNA regions and time after insertion of TEs into the genome and/or their chromosomal location. Here we addressed these issues using soybean retrotransposon SORE-1. We analyzed SORE-1 , inserted in exon 1 of the GmphyA2 gene, one of the newest insertions in this family so far identified. Cytosine methylation was detected in this element but was barely present in the adjacent regions. These results were correlated, respectively, with the presence and absence of the production of short interfering RNAs. Cyto-sine methylation profiles of 74 SORE-1 elements in the Williams 82 reference genome indicated that methylation frequency in the adjacent regions of SORE-1 was profoundly higher in pericentromeric regions than in euchromatic chromosome arms and was only weakly correlated with the length of time after insertion into the genome. Notably, the higher level of methylation in the 5' adjacent regions of SORE-1 coincided with the presence of repetitive elements in pericentromeric regions. Together, these results suggest that epigenetic influence of SORE-1 on the adjacent regions is influenced by its location on the chromosome.

The generation of effector CD8+ T cells (TEFF) requires activation of naive CD8+ T cells (TN) by dendritic cells (DCs) within lymphoid tissue. To date, it remains elusive how the duration of TN-DC interactions and integration of activation signals are controlled in vivo. Here, we report that lymphoid stroma-secreted ligands for CCR7 constrained interaction duration by gradually inducing CD8+ T cell release from DCs. At late time points of interactions, CCR7 ligands repositioned the F-actin-promoting factor DOCK2 away from the DC interface to enable CD8+ T cell detachment, proliferation onset and acquisition of cytotoxicity. Lack of CCR7 signaling, as during ex vivo activation or in chronically inflamed lymphoid tissue, caused sustained T cell-DC interactions, and generated dysfunctional TEFF with high expression of inhibitory receptors, impaired antimicrobial activity, and poor recall responses. In sum, our findings uncover that lymphoid stromal chemokines act as built-in "disruptors" of T cell-DC interactions for long-term preservation of TEFF functionality. ### Competing Interest Statement The authors have declared no competing interest.

Impact of Treg depletion on LN HEV remodelling

LSFM imaging of Treg depleted and T-cell depleted fibrosarcomas.

Tissue-resident CD8 + T cells (T RM ) continuously scan peptide-MHC (pMHC) complexes in their organ of residence to intercept microbial invaders. Recent data showed that T RM lodged in exocrine glands scan tissue in the absence of any chemoattractant or adhesion receptor signaling, thus bypassing the requirement for canonical migration-promoting factors. The signals eliciting this noncanonical motility and its relevance for organ surveillance have remained unknown. Using mouse models of viral infections, we report that exocrine gland T RM autonomously generated front-to-back F-actin flow for locomotion, accompanied by high cortical actomyosin contractility, and leading-edge bleb formation. The distinctive mode of exocrine gland T RM locomotion was triggered by sensing physical confinement and was closely correlated with nuclear deformation, which acts as a mechanosensor via an arachidonic acid and Ca 2+ signaling pathway. By contrast, naïve CD8 + T cells or T RM surveilling microbe-exposed epithelial barriers did not show mechanosensing capacity. Inhibition of nuclear mechanosensing disrupted exocrine gland T RM scanning and impaired their ability to intercept target cells. These findings indicate that confinement is sufficient to elicit autonomous T cell surveillance in glands with restricted chemokine expression and constitutes a scanning strategy that complements chemosensing-dependent migration.

Global overview of intra-tumoral HEVs in a 4T1 regressor tumour following PI-3065 treatment.

2D assessment of fibrosarcoma establishment on LN HEVs

Global overview of intra-tumoral HEVs in a 4T1 regressor tumour following PI-3065 treatment.

Impact of Treg depletion and LTβR agonist treatment on the immune cell organisation in fibrosarcoma tumours.

LSFM imaging of Treg depleted fibrosarcomas.

Members of the Regulator of G-protein signaling (Rgs) family regulate the extent and timing of G protein signaling by increasing the GTPase activity of Gα protein subunits. The Rgs family member Rgs1 is one of the most up-regulated genes in tissue-resident memory (TRM) T cells when compared to their circulating T cell counterparts. Functionally, Rgs1 preferentially deactivates Gαq, and Gαi protein subunits and can therefore also attenuate chemokine receptor-mediated immune cell trafficking. The impact of Rgs1 expression on tissue-resident T cell generation, their maintenance, and the immunosurveillance of barrier tissues, however, is only incompletely understood. Here we report that Rgs1 expression is readily induced in naïve OT-I T cells in vivo following intestinal infection with Listeria monocytogenes-OVA. In bone marrow chimeras, Rgs1-/- and Rgs1+/+ T cells were generally present in comparable frequencies in distinct T cell subsets of the intestinal mucosa, mesenteric lymph nodes, and spleen. After intestinal infection with Listeria monocytogenes-OVA, however, OT-I Rgs1+/+ T cells outnumbered the co-transferred OT-I Rgs1-/- T cells in the small intestinal mucosa already early after infection. The underrepresentation of the OT-I Rgs1-/- T cells persisted to become even more pronounced during the memory phase (d30 post-infection). Remarkably, upon intestinal reinfection, mice with intestinal OT-I Rgs1+/+ TRM cells were able to prevent the systemic dissemination of the pathogen more efficiently than those with OT-I Rgs1-/- TRM cells. While the underlying mechanisms are not fully elucidated yet, these data thus identify Rgs1 as a critical regulator for the generation and maintenance of tissue-resident CD8+ T cells as a prerequisite for efficient local immunosurveillance in barrier tissues in case of reinfections with potential pathogens.

Global overview of intra-tumoral HEVs in a 4T1 non-regressor tumour following PI-3065 treatment.

Global overview of intra-tumoral HEVs in 4T1 tumours following PI-3065 treatment.

SignificanceThe CD169+macrophages that play an important role in the fight against infections and cancer are receptive to environmental signals for their differentiation. We show that lymph node and splenic CD169+macrophages require both LTβR and RANK signaling since the conditional deficiency of either receptor results in their disappearance. Using a reporter mouse, we observe RANKL expression by a splenic mesenchymal cell subset and show that it participates in CD169+macrophage differentiation. Their absence leads to a reduced viral capture and a greatly attenuated virus-specific CD8+T cell expansion. Thus, tight control mechanisms operate for the precise positioning of these macrophages at sites where numerous immune-stimulatory forces converge.