Miracle-dz/UniFAR-FTUs huggingface dataset:
Morphological Characterization of the Seedlings of Short-root Mutant LM10 Selected from Rice (Oryza sativa L., cv. IR8)

We report the characterization of seedlings of LM10 which is one of the four short-root mutants derived from an M2 population of rice (Oryza sativa L., cv. IR8) seeds treated with NaN3. The morphological characteristics in the M3 generation of LM10 was the same as their M2 and there was no segregation in M3. The lengths of the seminal root, the crown root and the lateral root of LM10 seedlings were significantly shorter than those of IR8, but the number of crown roots and the density of lateral roots were higher in LM10. There was no difference in plant length between the two. The embryo and the radicle length of the mature embryo were shorter in LM10, but no difference was observed in the plumule. The cortex cell length of the maturation zone was remarkably shorter in LM10 than in IR8, though cell division of the meristem zone was normal in the two. Although it is well known that the shoot and root growth of the wild-type are inhibited by light exposure compared to dark, root growth of IM10 was accelerated by light exposure, but shoot growth was inhibited. These results indicated that LM10 is different from mutants reported previously in rice and represents a new mutant concerning root growth of rice.
Three Forms of α-Glucosidase and a Glucoamylase from Aspergillus awamori

Aspergillus awamori produced multiple forms (isoenzymes) of α-glucosidase, three of which could be separated from one another by DEAE-cellulose column chromatography, and a glucoamylase. The α-glucosidases isolated were designated as α-glucosidase I, α-glucosidase II and α-glucosidase III. They were homogeneous on gel electrofocusing and ultracentrifugation, respectively. The glucoamylase preparation was homogeneous on disc gel electrophoresis, gel electrofocusing and ultracentrifugation. The molecular weight of α-glucosidase I, α-glucosidase II, and α-glucosidase III, and glucoamylase was 125,000, 140,000, 130,000 and 88,000 to 83,700, respectively. The three α-glucosidases hydrolyzed maltose, maltotriose, phenyl α-maltoside, isomaltose, panose, phenyl α-glucoside, and amylose liberating glucose, but did not act on sucrose. Glucoamylase hydrolyzed maltose, maltotriose, phenyl α-maltoside, soluble starch, amylose, amylopectin, and glycogen, and glucose was the sole product formed in the digests of these s.
A Subtype of Adult-Born Neuron in Male Zebra Finch HVC Expresses DARPP-32 and Does Not Project to RA as part of the Vocal Motor Pathway

Adult male zebra finches (Taeniopygia guttata) continually incorporate adult-born neurons into HVC, a telencephalic brain region necessary for the production of learned song. These neurons express immediate early genes following song production, suggesting a role for neurogenesis in song production throughout the lifespan. Half of these adult-born HVC neurons (HVC NNs) send their axons to RA as part of the vocal motor pathway underlying learned song production, but the other half do not, and their identity remains unknown. Here we used cell birth-dating, retrograde tract tracing, and immunofluorescence to demonstrate that half of all HVC NNs express the neuron-specific phosphoprotein DARPP-32, a protein associated with DA receptor expression. We also demonstrate that DARPP-32+ HVC NNs are contacted by tyrosine hydroxylase immunoreactive fibers suggesting that they receive catecholaminergic input, are transiently larger than DARPP-32-negative HVC NNs, and do not send axons to RA as part of the vocal motor pathway. Taken together, these findings indicate the existence of a class of HVC NNs that do not project to RA and may constitute the aforementioned unknown half of all HVC NNs.
Phenotypic and functional characterization of first-trimester human placental macrophages, Hofbauer cells

Hofbauer cells (HBC) are a population of macrophages found in high abundance within the stroma of the first trimester human placenta. HBC are the only fetal immune cell population within the stroma of healthy placenta. However, the functional properties of these cells are poorly described. Aligning with their predicted origin via primitive haematopoiesis, we find that HBC are transcriptionally similar to yolk sac macrophages. Phenotypically, HBC can be identified as HLA-DR-FOLR2+ macrophages. We identify a number of factors HBC secrete (including IL-8 and MMP-9) that could affect placental angiogenesis and remodelling. We determine that HBC have the capacity to play a defensive role, where they are responsive to Toll-like receptor stimulation and are microbicidal. Finally, we also identify a population of placenta-associated maternal macrophages (PAMM1a) that adhere to the placental surface and express factors, such as fibronectin, that may aid in repair. Summary Using transcriptomic and proteomic data, Thomas, J. et al, analyse human first trimester placental macrophages and delineate markers that identify them. They also reveal that Hofbauer cells have microbicidal capacity, providing the fetus with an additional layer of protection from certain microbes. One sentence summary Hofbauer cells are primitive placental macrophages with a unique phenotype and role in fetal defence. Non-standard abbreviation Placental associated maternal monocytes/macrophages, PAMM.
Low cost conservation: Fishing gear threats to marine species

Understanding conflicts between objectives of fisheries and conservation is the key to finding win-win situations for marine biodiversity and fishers. Many marine species are threatened by harmful interactions with fisheries, but the threats they face are associated with the fishing gear used. Here, we undertake a novel analysis of marine species and their gear-specific threats to evaluate conservation-fisheries trade-offs to identify areas with high competing goals. Our analysis suggests that gillnet and longline fisheries pose the greatest risk to marine species yet deliver relatively low profits, emphasizing the inefficiencies of these gears. We find that the majority of the high seas has low economic fisheries benefits with over 25% of the high seas categorized as areas of ‘conservation prioritisation’ over fisheries.
To Close or to Collapse: The Role of Charges on Membrane Stability upon Pore Formation

Resealing of membrane pores is crucial for cell survival. We studied the membrane surface charge and medium composition as defining regulators triggering bursting and collapse of giant unilamellar vesicles upon poration. The pores were generated by either electric field or a detergent. Vesicles composed of mixtures of zwitterionic and negatively charged lipids at varying molar ratios were subjected to a single strong electric pulse and their response was characterized for a given membrane and medium composition. We observe that charged vesicles are prone to catastrophic vesicle collapse transforming them into tubular structures. The spectrum of destabilization responses includes the generation of long-living submicroscopic pores and partial vesicle bursting. The origin of these phenomena is related to the membrane edge tension, which governs pore closure. This edge tension significantly decreases as a function of the molar fraction of charged lipids. Destabilization of charged vesicles upon pore formation is a universal process since it is also observed with other poration stimuli. Disruption propensity is enhanced for membranes made of lipids with higher degree of unsaturation. It can be reversed by screening membrane charge in the presence of calcium ions. We interpret the observed findings in light of theories of stability and curvature generation in charged membranes and discuss mechanisms acting in cells to prevent total membrane collapse upon poration. Enhanced membrane stability is crucial for the success of electroporation-based technologies for cancer treatment and gene transfer. Significance Statement Leaky membranes cannot support life. Cells have developed protective mechanisms to respond to pore formation in their membranes. We find that essential membrane components such as (asymmetrically distributed) charged lipids destabilize the membrane upon poration and lead to catastrophic collapse, shown here on giant unilamellar vesicles as model membranes porated either by electric fields or detergent. The charged lipids act via reducing the pore edge tension. The membrane destabilization can be reverted by calcium ions and is less pronounced for lipids with lower degree of unsaturation. The observed membrane stabilization can be employed for optimizing biotechnological developments employing electroporation for cancer treatment.
An important role of the interplay between Bdnf transcription and histone acetylation in epileptogenesis

Brain-Derived Neurotrophic Factor is one of the most important trophic proteins in the brain. The role of this growth factor in neuronal plasticity, in health and disease, has been extensively studied. However, mechanisms of epigenetic regulation of Bdnf gene expression in epilepsy are still elusive. In our previous work, using a rat model of neuronal activation upon kainate-induced seizures, we observed a repositioning of Bdnf alleles from the nuclear periphery towards the nuclear center. This change of Bdnf intranuclear position was associated with transcriptional gene activity. In the present study, using the same neuronal activation model, we analyzed the relation between the percentage of the Bdnf allele at the nuclear periphery and clinical and morphological traits of epilepsy. We observed that the decrease of the percentage of the Bdnf allele at the nuclear periphery correlates with stronger mossy fiber sprouting - an aberrant form of excitatory circuits formation. Moreover, using in vitro hippocampal cultures we showed that Bdnf repositioning is a consequence of the transcriptional activity. Inhibition of RNA polymerase II activity in primary cultured neurons with Actinomycin D completely blocked Bdnf gene transcription and repositioning observed after neuronal excitation. Interestingly, we observed that histone deacetylases inhibition with Trichostatin A induced a slight increase of Bdnf gene transcription and its repositioning even in the absence of neuronal excitation. Presented results provide novel insight into the role of BDNF in epileptogenesis. Moreover, they strengthen the statement that this particular gene is a good candidate to search for a new generation of antiepileptic therapies.
CENP-A chromatin prevents replication stress at centromeres to avoid structural aneuploidy

Significance CENP-A, the histone H3 variant that forms a unique centromeric chromatin, is essential for faithful chromosome segregation during mitosis. Inability to connect the centromere to the mitotic spindle causes aneuploidy, a hallmark of many cancers. In addition to chromosome missegregation, chromosome fusions at (peri)centromeres are prevalent in cancers, but how such rearrangements arise remains unclear. Here, we identified a role for CENP-A in maintaining the integrity of centromere-associated repetitive sequences by ensuring their effective replication in human cells. In the absence of CENP-A, generation of DNA–RNA hybrids due to transcription–replication conflicts causes delayed DNA replication, centromere breakage, recombination, and chromosome translocations at centromeres. Centromeres thus possess a special mechanism to facilitate their replication and suppress chromosome translocations. Chromosome segregation relies on centromeres, yet their repetitive DNA is often prone to aberrant rearrangements under pathological conditions. Factors that maintain centromere integrity to prevent centromere-associated chromosome translocations are unknown. Here, we demonstrate the importance of the centromere-specific histone H3 variant CENP-A in safeguarding DNA replication of alpha-satellite repeats to prevent structural aneuploidy. Rapid removal of CENP-A in S phase, but not other cell-cycle stages, caused accumulation of R loops with increased centromeric transcripts, and interfered with replication fork progression. Replication without CENP-A causes recombination at alpha-satellites in an R loop-dependent manner, unfinished replication, and anaphase bridges. In turn, chromosome breakage and translocations arise specifically at centromeric regions. Our findings provide insights into how specialized centromeric chromatin maintains the integrity of transcribed noncoding repetitive DNA during S phase.
Pre-existing intratumoral CD8 T cells substantially contribute to control tumors following therapeutic anti-CD40 and polyI:C based vaccination

Background Dendritic cells are potently activated by the synergistic action of CD40 stimulation in conjunction with signaling through toll like receptors, subsequently activating antigen specific T cells. Cancer vaccines targeting the activation of dendritic cells in this manner show promise in murine models and are being developed for human cancer patients. While vaccine efficacy has been established, further investigation is needed to understand the mechanism of tumor control and how vaccination alters tumor infiltrating immune cells. Methods Mice bearing established murine melanoma tumors were vaccinated with agonist anti-CD40, polyI:C, and tumor antigen. Intratumoral T cell numbers, differentiation state, proliferation, and survival were assessed by flow cytometry. T cell effector function was measured both within the tumor and ex vivo by flow cytometry. T cell trafficking was blocked to examine changes to intratumoral T cells present at the time of vaccination. Results Vaccination led to increased intratumoral T cell numbers and delayed tumor growth. Expansion of T cells and tumor control did not require trafficking of T cells from the periphery. The increase in intratumoral T cells was associated with an acute burst in proliferation but not changes in viability. Intratumoral T cells had lower PD-1 and Eomes expression but were less functional after vaccination on a per cell basis. However, the increased intratumoral T cell numbers yielded increased effector T cells per tumor. Conclusions Pre-infiltrated CD8 T cells are responsive to CD40/TLR-mediated vaccination and sufficient for vaccination to delay tumor growth when additional T cell trafficking is blocked. This indicates that the existing T cell response and intratumoral DC could be critical for vaccination efficacy. This also suggests that circulating T cells may not be an appropriate biomarker for vaccination efficacy.
Accurately Clustering Single-cell RNA-seq data by Capturing Structural Relations between Cells through Graph Convolutional Network

Recent advances in single-cell RNA sequencing (scRNA-seq) technologies provide a great opportunity to study gene expression at cellular resolution, and the scRNA-seq data has been routinely conducted to unfold cell heterogeneity and diversity. A critical step for the scRNA-seq analyses is to cluster the same type of cells, and many methods have been developed for cell clustering. However, existing clustering methods are limited to extract the representations from expression data of individual cells, while ignoring the high-order structural relations between cells. Here, we proposed a new method (GraphSCC) to cluster cells based on scRNA-seq data by accounting structural relations between cells through a graph convolutional network. The representation learned from the graph convolutional network, together with another representation output from a denoising autoencoder network, are optimized by a dual self-supervised module for better cell clustering. Extensive experiments indicate that GraphSCC model outperforms state-of-the-art methods in various evaluation metrics on both simulated and real datasets. Further visualizations show that GraphSCC provides representations for better intra-cluster compactness and inter-cluster separability.
Maturation of telomere 3’-overhangs is linked to the replication stress response

Passage of the replication fork through telomeric repeats necessitates additional DNA processing by DNA repair factors, to regenerate the terminal 3’-overhang structure at leading telomeres. These factors are prevented from promoting telomeric recombination or fusion by an uncharacterized mechanism. Here we show that Rad5, a DNA helicase and ubiquitin ligase involved in the DNA damage tolerance pathway, participates in this mechanism. Rad5 is enriched at telomeres during telomere replication. Accelerated senescence seen in the absence of telomerase and Rad5, can be compensated for by a pathway involving the Rad51 recombinase and counteracted by the helicase Srs2. However, this pathway is only active at short telomeres. Instead, the ubiquitous activity of Rad5 during telomere replication is necessary for the proper reconstitution of the telomeric 3’-overhang, indicating that Rad5 is required to coordinate telomere maturation during telomere replication.
Engineering High-Yield Biopolymer Secretion Creates an Extracellular Protein Matrix for Living Materials

Engineered living materials (ELM) aim to mimic characteristics of natural occurring systems, bringing the benefits of self-healing, synthesis, autonomous assembly, and responsiveness to traditional materials. Previous research has shown the potential of replicating the bacterial extracellular matrix (ECM) to mimic biofilms. ABSTRACT The bacterial extracellular matrix forms autonomously, giving rise to complex material properties and multicellular behaviors. Synthetic matrix analogues can replicate these functions but require exogenously added material or have limited programmability. Here, we design a two-strain bacterial system that self-synthesizes and structures a synthetic extracellular matrix of proteins. We engineered Caulobacter crescentus to secrete an extracellular matrix protein composed of an elastin-like polypeptide (ELP) hydrogel fused to supercharged SpyCatcher [SC(−)]. This biopolymer was secreted at levels of 60 mg/liter, an unprecedented level of biomaterial secretion by a native type I secretion apparatus. The ELP domain was swapped with either a cross-linkable variant of ELP or a resilin-like polypeptide, demonstrating this system is flexible. The SC(−)-ELP matrix protein bound specifically and covalently to the cell surface of a C. crescentus strain that displays a high-density array of SpyTag (ST) peptides via its engineered surface layer. Our work develops protein design guidelines for type I secretion in C. crescentus and demonstrates the autonomous secretion and assembly of programmable extracellular protein matrices, offering a path forward toward the formation of cohesive engineered living materials. IMPORTANCE Engineered living materials (ELM) aim to mimic characteristics of natural occurring systems, bringing the benefits of self-healing, synthesis, autonomous assembly, and responsiveness to traditional materials. Previous research has shown the potential of replicating the bacterial extracellular matrix (ECM) to mimic biofilms. However, these efforts require energy-intensive processing or have limited tunability. We propose a bacterially synthesized system that manipulates the protein content of the ECM, allowing for programmable interactions and autonomous material formation. To achieve this, we engineered a two-strain system to secrete a synthetic extracellular protein matrix (sEPM). This work is a step toward understanding the necessary parameters to engineering living cells to autonomously construct ELMs.
Favipiravir-resistant influenza A virus shows potential for transmission

Favipiravir is a nucleoside analogue which has been licensed to treat influenza in the event of a new pandemic. We previously described a favipiravir resistant influenza A virus generated by in vitro passage in presence of drug with two mutations: K229R in PB1, which conferred resistance at a cost to polymerase activity, and P653L in PA, which compensated for the cost of polymerase activity. However, the clinical relevance of these mutations is unclear as the mutations have not been found in natural isolates and it is unknown whether viruses harbouring these mutations would replicate or transmit in vivo. Here, we infected ferrets with a mix of wild type p(H1N1) 2009 and corresponding favipiravir-resistant virus and tested for replication and transmission in the absence of drug. Favipiravir-resistant virus successfully infected ferrets and was transmitted by both contact transmission and respiratory droplet routes. However, sequencing revealed the mutation that conferred resistance, K229R, decreased in frequency over time within ferrets. Modelling revealed that due to a fitness advantage for the PA P653L mutant, reassortment with the wild-type virus to gain wild-type PB1 segment in vivo resulted in the loss of the PB1 resistance mutation K229R. We demonstrated that this fitness advantage of PA P653L in the background of our starting virus A/England/195/2009 was due to a maladapted PA in first wave isolates from the 2009 pandemic. We show there is no fitness advantage of P653L in more recent pH1N1 influenza A viruses. Therefore, whilst favipiravir-resistant virus can transmit in vivo, the likelihood that the resistance mutation is retained in the absence of drug pressure may vary depending on the genetic background of the starting viral strain. Author Summary In the event of a new influenza pandemic, drugs will be our first line of defence against the virus. However, drug resistance has proven to be particularly problematic to drugs against influenza. Favipiravir is a novel drug which might be used against influenza virus in the event of a new pandemic. Is resistance likely to be a problem for the use of favipiravir? Our previous work has shown that resistance to favipiravir can be generated in cell culture but we don’t know whether there will be a cost preventing the spread of resistance in whole organisms. Here, we used a mix of wild-type and resistant influenza viruses from early in the 2009 pandemic to test whether viruses resistant to favipiravir could transmit between ferrets. We found that the resistant viruses could transmit but that the resistance mutation was selected against within some ferrets. Using modelling and in vitro experiments, we found that the resistant mutation was selected against in the influenza strain from our experiment but not in more recently evolved strains. Our results show that favipiravir resistant viruses could spread if resistance is generated but the probability will depend on the genetic background of the virus.
Feature-based encoding of face identity by single neurons in the human amygdala and hippocampus

Neurons in the human amygdala and hippocampus that are selective for the identity of specific people are classically thought to encode a person’s identity invariant to visual features (e.g., skin tone, eye shape). However, it remains largely unknown how visual information from higher visual cortical areas is translated into such a semantic representation of an individual person. Here, we show that some amygdala and hippocampal neurons are selective to multiple different unrelated face identities based on shared visual features. The encoded identities form clusters in the representation of a deep neural network trained to recognize faces. Contrary to prevailing views, these neurons thus represent an individual’s face with a visual feature-based code rather than one based on association with known concepts. Feature neurons encoded faces regardless of their identity, race, gender, familiarity, or pixel-level visual features; and the region of feature space to which feature neurons are tuned predicted their response to new face stimuli. Our results reveal a new class of neurons that bridge the perception-driven representation of facial features in the higher visual cortex with mnemonic semantic representations in the MTL, which may form the basis for declarative memory.