SUMMARY Differentiating cells can dedifferentiate to replace stem cells in aged or damaged tissues, but the underlying mechanisms are unknown. In the Drosophila testis a cluster of stromal cells called the hub creates a niche by locally activating Janus-Kinase, Signal Transducer and Activator of Transcription (Jak-STAT) signaling in adjacent germline and somatic stem cells. Here we establish a novel system to study spermatogonial dedifferentiation. Ectopically expressing the differentiation factor Bag-of-marbles (Bam) removes germline stem cells from the niche. However, withdrawing ectopic Bam causes interconnected spermatogonia to fragment, move into the niche, exchange positions with resident somatic stem cells and establish contact with the hub. Concomitantly, Actin-based protrusions appear on subsets of spermatogonia, suggesting acquired motility. Furthermore, global downregulation of Jak-STAT signaling inhibits dedifferentiation, indicating that normal levels of pathway activation are required to promote movement of spermatogonia into the niche during dedifferentiation, where they outcompete somatic stem cells for niche occupancy.

SUMMARYAdult stem cells modulate their output by varying between symmetric and asymmetric divisions, but have rarely been observed in living intact tissues. Germline stem cells (GSCs) in the Drosophila testis are anchored to somatic hub cells and were thought to exclusively undergo oriented asymmetric divisions, producing one stem cell that remains hub-anchored and one daughter cell displaced out of the stem cell-maintaining micro-environment (niche). We developed extended live imaging of the Drosophila testis niche, allowing us to track individual germline cells. Surprisingly, new wild-type GSCs are generated in the niche during steady-state tissue maintenance by a previously undetected event we term 'symmetric renewal', where interconnected GSCdaughter cell pairs swivel such that both cells contact the hub. We also captured GSCs undergoing direct differentiation by detaching from the hub. Following starvation-induced GSC loss, GSC numbers are restored by symmetric renewals. Furthermore, upon more severe (genetically induced) GSC loss, both symmetric renewal and de-differentiation (where interconnected spermatogonia fragment into pairs while moving towards then establishing contact with the hub) occur simultaneously to replenish the GSC pool. Thus, stereotypically oriented stem cell divisions are not always correlated with an asymmetric outcome in cell fate, and changes in stem cell output are governed by altered signals in response to tissue requirements.

Summary Germline stem cells (GSCs) in Drosophila are descendants of primordial germ cells (PGCs) specified during embryogenesis. The precise timing of GSC establishment in the testis has not been determined, nor is it known whether mechanisms that control GSC maintenance in the adult are involved in GSC establishment. Here, we determine that PGCs in the developing male gonad first become GSCs at the embryo to larval transition. This coincides with formation of the embryonic hub; the critical signaling center that regulates adult GSC behavior within the stem cell microenvironment (niche). We find that the Jak-STAT signaling pathway is activated in a subset of PGCs that associate with the newly-formed embryonic hub. These PGCs express GSC markers and function like GSCs, while PGCs that do not associate with the hub begin to differentiate. In the absence of Jak-STAT activation, PGCs adjacent to the hub fail to exhibit the characteristics of GSCs, while ectopic activation of the Jak-STAT pathway prevents differentiation. These findings show that stem cell formation is closely linked to development of the stem cell niche, and suggest that Jak-STAT signaling is required for initial establishment of the GSC population in developing testes.

This article investigates the errors in supermolecule calculations for the helium dimer. In a full CI calculation, there are two errors. One is the basis set superposition error (BSSE), the other is the basis set convergence error (BSCE). Both of the errors arise from the incompleteness of the basis set. These two errors make opposite contributions to the interaction energies. The BSCE is by far the largest error in the short range and larger than (but much closer to) BSSE around the Van der Waals minimum. Only at the long range, the BSSE becomes the larger error. The BSCE and BSSE largely cancel each other over the Van der Waals well. Accordingly, it may be recommended to not include the BSSE for the calculation of the potential energy curve from short distance till well beyond the Van der Waals minimum, but it may be recommended to include the BSSE correction if an accurate tail behavior is required. Only if the calculation has used a very large basis set, one can refrain from including the counterpoise correction in the full potential range. These results are based on full CI calculations with the aug-cc-pVXZ (X = D, T, Q, 5) basis sets.

Epitaxial growth suffers from the mismatches in lattice and dangling bonds arising from different crystal structures or unit cell parameters. Here, we demonstrate the epitaxial growth of 2D MoS ribbon on 1D CdS nanowires (NWs) via surface and subsurface defects. The interstitial Cd in the (12̅10) crystal plane of the [0001]-oriented CdS NWs are found to serve as nucleation sites for interatomically bonded [001]-oriented MoS, where the perfect lattice match (∼99.7%) between the (101̅1) plane of CdS and the (002)-faceted in-plane MoS result in coaxial MoS ribbon/CdS NWs heterojunction. The coaxial but heterotropic epitaxial MoS ribbon on the surface of CdS NWs induces delocalized interface states that facilitate charge transport and the reduced surface state. A less than 5-fold ribbon width of MoS as hydrogen evolution cocatalyst exhibits a ∼10-fold H evolution enhancement than state of the art Pt in an acidic electrolyte, and apparent quantum yields of 79.7% at 420 nm, 53.1% at 450 nm, and 9.67% at 520 nm, respectively.

Establishment and maintenance of functional stem cells is critical for organ development and tissue homeostasis. Little is known about the mechanisms underlying stem establishment during organogenesis. Drosophila testes are among the most thoroughly characterized systems for studying stem cell behavior, with germline stem cells (GSCs) and somatic cyst stem cells (CySCs) cohabiting a discrete stem cell niche at the testis apex. GSCs and CySCs are arrayed around hub cells that also comprise the niche and communication between hub cells, GSCs, and CySCs regulates the balance between stem cell maintenance and differentiation. Recent data has shown that functional, asymmetrically dividing GSCs are first established at ~23 hrs after egg laying during Drosophila testis morphogenesis (Sheng et al., 2009). This process correlates with coalescence of the hub, but development of CySCs from somatic gonadal precursors (SGPs) was not examined. Here, we show that functional CySCs are present at the time of GSC establishment, and that Jak-STAT signaling is necessary and sufficient for CySC maintenance shortly thereafter. Furthermore, hyper-activation of Jak in CySCs promotes expansion of the GSC population, while ectopic Jak activation in the germline induces GSC gene expression in GSC daughter cells but does not prevent spermatogenic differentiation. Together, these observations indicate that, similar to adult testes, Jak-STAT signaling from the hub acts on both GSCs and CySC to regulate their development and differentiation, and that additional signaling from CySCs to the GSCs play a dominant role in controlling GSC maintenance during niche formation.

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A stepwise four‐electron reaction significantly alleviates the thermodynamics reaction barrier for overall water splitting. Regenerated 1D carbon nitride nanowire bundles from tailoring and reassembly of 2D g‐C3N4 produce novel physicochemical and optoelectronic properties, which well realize the stepwise four‐electron reaction along with a quantum efficiency of 5.2‰ at 420 nm.