bluuebunny/crossref_metadata_2025_split huggingface dataset:
Phenotypic plasticity, life cycles, and the evolutionary transition to multicellularity
Authors: Tang Si , Pichugin Yuriy , Hammerschmidt Katrin 
Published: October 2021

SUMMARYUnderstanding the evolutionary transition to multicellularity is a key problem in evolutionary biology (1–4). While around 25 independent instances of the evolution of multicellular existence are known across the tree of life (5), the ecological conditions that drive such transformations are not well understood. The first known transition to multicellularity occurred approximately 2.5 billion years ago in cyanobacteria (5–7), and today’s cyanobacteria are characterized by an enormous morphological diversity, based upon which they have been classified into five sections. They range from single-celled species (section I), unicellular cyanobacteria with packet-like phenotypes, e.g., tetrads (section II) and simple filamentous species (section III) to highly differentiated filamentous ones (sections IV and V) (8–10). The unicellular cyanobacterium Cyanothece sp. ATCC 51142, an isolate from the intertidal zone of the U.S. Gulf Coast (11), has been classified as a section I species, and it phylogenetically clusters with the other N2-fixing unicellular cyanobacteria (12).Here we report a facultative multicellular life cycle for a unicellular cyanobacterium, where multicellular filaments and unicellular stages alternate. In a series of experiments we identify the environmental factors underlying the phenotypic switch between the two morphologies. Then we experimentally confirm that the dissolution of filaments into solitary cells is triggered by changes in the external environment, which in turn is modified by the Cyanothece cells. Finally, using numerical models, we test a number of hypotheses regarding the nature of the environmental cues and the physical mechanisms underlying filament dissolution. While results predict that the observed response can be caused by an excreted compound in the medium, we cannot fully exclude changes in nutrient availability (as in (13,14)). The best-fit modeling results demonstrate a nonlinear effect of the compound, which is characteristic for density-dependent sensing systems (15,16). Further, filament fragmentation is predicted to occur by means of connection cleavage rather than by cell death of every alternate cell, which is corroborated by results from fluorescent and scanning electron microscopy. The phenotypic switch between the single-celled and multicellular morphology constitutes an environmentally dependent life cycle, which likely represents an important step en route to permanent multicellularity.
Extracellular matrix stiffness and TGFβ2 regulate YAP/TAZ activity in human trabecular meshwork cells
Authors: Li Haiyan , Raghunathan VijayKrishna , Stamer W. Daniel , Ganapathy Preethi S. , Herberg Samuel 
Published: October 2021

AbstractPrimary open-angle glaucoma progression is associated with increased human trabecular meshwork (HTM) stiffness and elevated transforming growth factor beta 2 (TGFβ2) levels in aqueous humor. Increased transcriptional activity of Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ), central players in mechanotransduction, are implicated in glaucomatous HTM (GTM) cell dysfunction. Yet, the detailed mechanisms underlying YAP/TAZ modulation in HTM cells in response to alterations in extracellular matrix (ECM) stiffness and TGFβ2 levels are not well understood. Using biomimetic ECM hydrogels with tunable stiffness, here we show that increased ECM stiffness elevates YAP/TAZ transcriptional activity potentially through modulating focal adhesions and cytoskeletal rearrangement. Furthermore, TGFβ2 increased YAP/TAZ nuclear localization in both normal and glaucomatous HTM cells, which was prevented by inhibiting extracellular-signal-regulated kinase and Rho-associated kinase signaling pathways. Filamentous (F)-actin depolymerization reversed TGFβ2-induced YAP/TAZ nuclear localization. YAP/TAZ depletion using siRNA or verteporfin decreased focal adhesions, ECM remodeling and cell contractile properties. Similarly, YAP/TAZ inactivation with verteporfin partially blocked TGFβ2-induced HTM/GTM hydrogel contraction and stiffening. Collectively, our data provide evidence for a pathologic role of aberrant YAP/TAZ signaling in glaucomatous HTM cell dysfunction, and may help inform strategies for the development of novel multifactorial approaches to prevent progressive ocular hypertension in glaucoma.
Strong spatial population structure shapes the temporal coevolutionary dynamics of costly female preference and male display
Authors: Tschol Maximilian , Reid Jane M. , Bocedi Greta 
Published: October 2021

AbstractFemale mating preferences for exaggerated male display traits are commonplace. Yet, comprehensive understanding of the evolution and persistence of costly female preference through indirect (Fisherian) selection in finite populations requires some explanation for the persistence of additive genetic variance (Va) underlying sexual traits, given that directional preference is expected to deplete Va in display and hence halt preference evolution. However, the degree to which Va, and hence preference-display coevolution, may be prolonged by spatially variable sexual selection arising solely from limited gene flow and genetic drift within spatially structured populations has not been examined. Our genetically and spatially explicit model shows that spatial population structure arising in an ecologically homogeneous environment can facilitate evolution and long-term persistence of costly preference given small subpopulations and low dispersal probabilities. Here, genetic drift initially creates spatial variation in female preference, leading to persistence of Va in display through “migration-bias” of genotypes maladapted to emerging local sexual selection, thus fuelling coevolution of costly preference and display. However, costs of sexual selection increased the probability of subpopulation extinction, limiting persistence of high preference-display genotypes. Understanding long-term dynamics of sexual selection systems therefore requires joint consideration of coevolution of sexual traits and metapopulation dynamics.
A kinase-dead Csf1r mutation associated with adult-onset leukoencephalopathy has a dominant-negative impact on CSF1R signaling
Authors: Stables Jennifer , Green Emma K. , Sehgal Anuj , Patkar Omkar , Keshvari Sahar , Taylor Isis , Ashcroft Maisie E. , Grabert Kathleen , Wollscheid-Lengeling Evi , Szymkowiak Stefan , McColl Barry W. , Adamson Antony , Humphreys Neil E. , Mueller Werner , Starobova Hana , Vetter Irina , Shabestari Sepideh Kiani , Blurton-Jones Matthew M. , Summers Kim M. , Irvine Katharine M. , Pridans Clare , Hume David A. 
Published: October 2021

AbstractAmino acid substitutions in the kinase domain of the human CSF1R gene are associated with autosomal dominant adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP). To model the human disease, we created a disease-associated mutation (Glu631Lys; E631K) in the mouse Csf1r locus. Homozygous mutation (Csf1rE631K/E631K) phenocopied the Csf1r knockout; with prenatal mortality or severe postnatal growth retardation and hydrocephalus. Heterozygous mutation delayed the postnatal expansion of tissue macrophage populations in most organs. Bone marrow cells from Csf1rE631K/+ mice were resistant to CSF1 stimulation in vitro, and Csf1rE631K/+ mice were unresponsive to administration of a CSF1-Fc fusion protein which expands tissue macrophage populations in controls. In the brain, microglial cell numbers and dendritic arborization were reduced in the Csf1rE631K/+ mice as in ALSP patients. The microglial phenotype is the opposite of microgliosis observed in Csf1r+/- mice. However, we found no evidence of brain pathology or impacts on motor function in aged Csf1rE631K/+ mice. We conclude that disease-associated CSF1R mutations encode dominant negative repressors of CSF1R signaling. We speculate that leukoencephalopathy associated with human CSF1R mutations requires an environmental trigger and/or epistatic interaction with common neurodegenerative disease-associated alleles.Summary StatementThis study describes the effect of a human disease-associated mutation in the mouse CSF1R gene on postnatal development and growth factor responsiveness of cells of the macrophage lineage.
Progranulin deficiency results in reduced bis(monoacylglycero)phosphate (BMP) levels and gangliosidosis
Authors: Boland Sebastian , Swarup Sharan , Ambaw Yohannes A. , Richards Ruth C. , Fischer Alexander W. , Singh Shubham , Aggarwal Geetika , Spina Salvatore , Nana Alissa L. , Grinberg Lea T. , Seeley William W. , Surma Michal A. , Klose Christian , Paulo Joao A. , Nguyen Andrew D. , Harper J. Wade , Walther Tobias C. , Farese Robert V. 
Published: October 2021

SUMMARYHomozygous mutations of granulin precursor (GRN) lead to neuronal ceroid lipofuscinosis1, a severe neurodevelopmental disease, in humans and neuroinflammation in mice2. Haploinsufficiency of GRN almost invariably causes frontotemporal dementia (FTD)3,4. The GRN locus produces progranulin (PGRN), a lysosomal precursor protein that is cleaved to granulin peptides5,6. Despite intensive investigation, the function of granulins and the reason why their absence causes neurodegeneration remain unclear. Here, we investigated PGRN function in lipid degradation, a major function of lysosomes. We show that PGRN-knockout human cells, PGRN-deficient murine brain, and frontal lobes of human brains from patients with GRN mutation-related FTD have increased levels of gangliosides, highly abundant sialic acid–containing glycosphingolipids (GSL) that are degraded in lysosomes. Probing how PGRN deficiency causes these changes, we found normal levels and activities of enzymes that catabolize gangliosides. However, levels of bis(monoacylglycero)phosphate (BMP), a lysosomal lipid required for ganglioside catabolism7, were markedly reduced in PGRN-deficient cells and patient brain tissues. These data indicate that granulins are required to maintain BMP levels, which regulate ganglioside catabolism, and that PGRN deficiency in lysosomes leads to gangliosidosis. This aberrant accumulation of gangliosides may contribute to neuroinflammation and neurodegeneration susceptibility.
Serum glycoprotein markers in non-alcoholic steato-hepatitis and hepatocellular carcinoma
Authors: Ramachandran Prasanna , Xu Gege , Huang Hector H. , Rice Rachel , Zhou Bo , Lind-paintner Klaus , Serie Daniel 
Published: October 2021

AbstractFatty liver disease progresses through stages of fat accumulation and inflammation to non-alcoholic steatohepatitis (NASH), fibrosis and cirrhosis and eventually hepatocellular carcinoma (HCC). Currently available diagnostic tools for HCC lack sensitivity and specificity and deliver little value to patients. In this study, we investigated the use of circulating serum glycoproteins to identify a panel of potential prognostic markers that may be indicative of progression from the healthy state to NASH and further to HCC. Serum samples were processed using a standard pre-analytical sample preparation protocol and were analyzed using a novel high throughput glycoproteomics platform. We analyzed 413 glycopeptides, representing 57 abundant serum proteins and compared among the three phenotypes. Our initial dataset contained healthy, NASH, and HCC serum samples. We analyzed normalized abundance of common glycoforms and found 40 glycopeptides with statistically significant differences in abundances in NASH and HCC compared to controls. Summary level relative abundance of core-fucosylated, sialylated and branched glycans containing glycopeptides were higher in NASH and HCC as compared to controls. We replicated some of our findings in an independent set of samples of individuals with benign liver conditions and HCC, respectively. Our results may be of value in the management of liver diseases.TOC only
TES-1/Tes protects junctional actin networks under tension from self-injury during epidermal morphogenesis in the C. elegans embryo
Authors: Lynch Allison M. , Lucas Bethany G. , Winkelman Jonathan D. , Martin Sterling C.T. , Block Samuel D. , Audhya Anjon , Gardel Margaret L. , Hardin Jeff 
Published: October 2021

AbstractDuring embryonic morphogenesis, the integrity of epithelial tissues depends on the ability of cells in tissue sheets to undergo rapid changes in cell shape while preventing self-injury to junctional actin networks. LIM domain-containing repeat (LCR) proteins are recruited to sites of strained actin filaments in cultured cells [1–3], and are therefore promising candidates for mediating self-healing of actin networks, but whether they play similar roles in living organisms has not been determined. Here, we establish roles for Caenorhabditis elegans TES-1/Tes, an actin-binding LCR protein present at apical junctions, during epithelial morphogenesis. TES-1::GFP is recruited to apical junctions during embryonic elongation, when junctions are under tension; in embryos in which stochastic failure of cell elongation occurs, TES-1 is only strongly recruited to junctions in cells that successfully elongate, and recruitment is severely compromised in genetic backgrounds in which cell shape changes do not successfully occur. tes-1 mutant embryos display junctional F-actin defects, and loss of TES-1 strongly enhances tension-dependent injury of junctional actin networks in hypomorphic mutant backgrounds for CCC components, suggesting that TES-1 helps to prevent self-injury of junctional actin networks during rapid cell shape change. Consistent with such role, a fragment of TES-1 containing its LIM domains localizes to stress fiber strain sites (SFSS) in cultured vertebrate cells. Together, these data establish TES-1 as a tension-sensitive stabilizer of the junctional actin cytoskeleton during embryonic morphogenesis.
Crystal Structures of Ferritin Grown by the Microbatch Method in the Presence of Agarose and Electric Field Shows Enhanced Metal Binding
Authors: Seetharaman Aditya , Babu Priyadharshine Ramesh , Ismail Maham , Miller Darcie J , Stojanoff Vivian 
Published: October 2021

AbstractFerritin is an ubiquitous iron storage protein found in all kingdoms of life. Ferritin is essential for iron homeostasis and is involved in a wide range of physiological and pathological processes. Several structures of ferritin in complex with small molecules and metal ions have been reported. Here we report the crystal structures of Horse Spleen Ferritin, in which the crystals were grown by employing a novel approach adopting the microbatch experiments performed in the presence and absence of electric field using a 2% agarose pellet of CdSO4. We observed that 1) these structures contain increased number of Cd ions as compared to the crystallization of same protein by others using different methods. 2) The externally applied electric field reduced the number of nucleation and with fewer nucleation the size of the crystals increased. 3) There is no significant conformational change observed among these structures. 4) Irrespective of the externally applied electric field, this agarose microbatch crystallization method facilitates the retaining of increased number of bound metal ions with ferritin to mimic the possible in vivo environment.
Examining internet banking user’s continuance intention through the lens of technology continuance theory and task technology fit model
Authors: Rahi Samar , Abd Ghani Mazuri 
Published: October 2021

Purpose
The long-term success of internet banking (IB) services is connected with continuous use. Therefore, examining factors which influence IB user continuance intention is important. Grounded in technology continuance theory, bank transparency and task technology fit (TTF) model, the purpose of this study is to develop a unified technology continuance model to investigate IB user continuance intention.

Design/methodology/approach
The research model was empirically tested with 348 responses. Respondents included in this study had prior experience with IB services. For hypotheses testing, the structural equation modelling approach was used.

Findings
Findings indicate that the research model has substantial power in explaining IB user continuance intention. Importance performance matrix analysis revealed that bank transparency had the highest importance in determining IB user continuance intention. Therefore, factors like user satisfaction and perceived usefulness have shown a medium level of importance in determining IB user continuance intention. Satisfaction is influenced by perceived usefulness and confirmation and established a significant impact on IB user continuance intention.

Practical implications
The findings of this research are useful for bank managers and policymakers to develop and design IB services according to user’s expectations. Results demonstrate that expectation confirmation and perceived usefulness are antecedents of IB user satisfaction and IB user continuance intention. In addition to that bank, transparency has shown a significant effect on user expectation and IB user continuance intention. These findings established that accuracy in sharing bank information and clarity in transaction charges encourage the user to continue the use of IB services.

Originality/value
The current study develops a unified technology continuance model based on the TTF model and technology continuance theory and investigates IB user continuance intention. Moreover, bank transparency is added in the technology continuance model and established a significant impact towards user expectation confirmation and continuance intention. These findings contribute to the limited body of research in the context of IB user continuance intention and enrich information system literature.
The open innovation journey along heterogeneous modes of knowledge-intensive marketing collaborations: a cross-sectional study of innovative firms in Europe
Authors: Papa Armando , Mazzucchelli Alice , Ballestra Luca Vincenzo , Usai Antonio 
Published: October 2021

PurposePrevious research focused on open innovation (OI) suggests that enterprises benefit from adopting the journey; however, the relationship among OI, marketing journey and knowledge-intensive innovation marketing activities (KIIMA) remains unclear. The present study proposes a conceptual model of the marketing journey linking heterogeneous modes of marketing collaboration to knowledge-intensive activities.Design/methodology/approachThe conceptual model was tested via ordinary least squares (OLS) linear regression based on a sample of data drawn from the Eurostat database.FindingsThe results indicate that strategies are a robust proxy for evaluating KIIMA, and partnerships, heterogeneous sources of knowledge and different marketing modes for collaboration among European knowledge-intensive firms are core antecedents of KIIMA, such as new-product development and marketing innovation, as well as firms' sustainable competitive advantage.Originality/valueThis study fills the gap by tracking the role of the journey within marketing collaborations on KIIMA, and it intervenes in the debate about interactive marketing innovation mechanisms. The study contributes to OI, knowledge management and the marketing literature by identifying the heterogeneous modes for marketing collaborations under which the marketing journey enhances knowledge-intensive activities such as those for marketing innovation.
Placebo outsourcing: when does provider’s bluffing enhance customer satisfaction?
Authors: Florea Dorian Laurentiu , Barbu Cătălin Mihail , Rotea Claudia Cristina 
Published: October 2021

Purpose
Drawing on signaling theory, this paper aims to argue in favor of a “placebo outsourcing effect” (POE) consisting of a positive relationship between provider’s bluffing and customer satisfaction.

Design/methodology/approach
The authors applied prediction-oriented segmentation SEM on a dyadic sample of 171 outsourcing relationships.

Findings
The authors highlighted two segments that display a form of POE, representing about three-quarters of the customer-provider dyads. The first segment exhibits a positive relationship between the provider’s bluffing and customer satisfaction that is further strengthened by the provider’s reputation and customer’s operational capabilities, while for the other segment, the provider’s bluffing has positive interactions with both operational capabilities and outsourcing experience. These findings show that service providers have reached the bluffing proficiency that enables them to bluff customer firms with varying levels of operational capabilities and outsourcing experience by using the most appealing signals for every type of customer.

Practical implications
Based on the findings, the authors provided to customer firms extensive guidelines to avoid the POE by frustrating service provider’s bluffing proficiency.

Originality/value
This study’s originality resides in the amendment of the disconfirmation paradigm of satisfaction in the outsourcing context by introducing and testing the POE.
“Sub-debt trap”: a real effect of an ill-design adoption of basel accord in the Bangladeshi banking industry
Authors: Hasan A.K.M. Kamrul , Suzuki Yasushi 
Published: October 2021

Purpose
The purpose of this paper is to investigate the impact of basel accord on the Bangladeshi bank performance including Islamic banks and the role of subordinated debt (sub-debt) as basel regulatory capital (BRC).

Design/methodology/approach
The authors conducted the empirical investigation by adopting a quantitative approach and using the secondary data available in the annual reports of the sample banks between 2009 and 2018. This paper develops an econometric model to compare and analyze the regression result under two states of capital-to-risk adjusted assets ratio (CRAR) with sub-debt and CRAR without sub-debt. This paper analyzes the impact of sub-debt in the largest Islamic bank for the year 2007 as a case study for endorsing the findings.

Findings
This paper finds that CRAR has positive alignments with return on equity (ROE) and cash dividend when sub-debt is considered as Tier 2 capital. This paper observes that the huge bad loan write-off supports to downsize the asset size thus temporarily enhance the return on assets (ROA). In a nutshell, sub-debt gives banks an ill incentive to disburse steady cash dividends instead of injecting genuine equity capital, encouraging them to take more credit risk. In fact, more private commercial banks (PCBs) issued huge sub-debts between 2009 and 2018 under a unique arrangement, which the authors termed as the “sub-debt trap.”

Research limitations/implications
This paper draws policy implications for the banking regulator to identify and rectify a systemic problem of the “sub-debt trap” which hinders the regulatory purpose from the implementation of basel accord II and III. A limitation of this study is the authors shed analytical light on Bangladeshi banks, i.e. it a single country analysis which may not be generalized to other developing countries except matching with a similar context.

Originality/value
The paper contributes to accumulating empirical studies on the effectiveness of basel accord implementation in developing countries. In most of the developing countries, where institutional loopholes are a major concern, the research provides evidence that how weak institutional settings are largely responsible for harvesting the potential benefit from micro-prudential regulation such as the basel accord. To shed analytical light on developing country context, the study document that sub-debt has been instrumentalized to maintain minimum capital ratio and banks managers tends more focus on improving ROE instead of ROA. The findings of the study are supportive to other developing countries where sub-debt considered as BRC and issued through private placement. To the best of the authors’ knowledge, it is the first attempt to cast doubt on the impact of sub-debt as a BRC, given the uniqueness of the Bangladeshi banking industry, on the PCBs including Islamic banks.