The Formation of Massive Cluster Galaxies

We present composite 3.6 and 4.5 micron luminosity functions for cluster galaxies measured from the Spitzer Deep, Wide-Field Survey (SDWFS) for 0.3<z<2. We compare the evolution of m* for these luminosity functions to models for passively evolving stellar populations to constrain the primary epoch of star formation in massive cluster galaxies. At low redshifts (z < 1.3) our results agree well with models with no mass assembly and passively evolving stellar populations with a luminosity-weighted mean formation redshift zf=2.4 assuming a Kroupa initial mass function (IMF). We conduct a thorough investigation of systematic biases that might influence our results, and estimate systematic uncertainites of Delta zf=(+0.16-0.18) (model normalization), Delta zf=(+0.40-0.05) (alpha), and Delta zf=(+0.30-0.45) (choice of stellar population model). For a Salpeter type IMF, the typical formation epoch is thus strongly constrained to be z ~2-3. Higher formation redshifts can only be made consistent with the data if one permits an evolving IMF that is bottom-light at high redshift, as suggested by van Dokkum et al 2008. At high redshift (z > 1.3) we also witness a statistically significant (>5sigma) disagreement between the measured luminosity function and the continuation of the passive evolution model from lower redshifts. After considering potential systematic biases that might influence our highest redshift data points, we interpret the observed deviation as potential evidence for ongoing mass assembly at this epoch.Comment: 17 pages, 14 figures, accepted for publication in Ap

Reviewing Vietnam's Nationally Determined Contribution: A New Perspective Using the Marginal Cost of Abatement

The processes countries use to revise their Nationally Determined Contributions (NDCs) under the UNFCCC's Paris Agreement will be key to ensure that their pledges lead to effective climate change policy. In many developing countries, the agriculture, forestry and other land use (AFOLU) sector is central to their NDCs. For this study, a marginal abatement cost (MAC) curve was used to review Vietnam's mitigation pledges pertaining to the AFOLU sector. We conclude that Vietnam has the potential to increase its NDC pledges, especially in the land use sector and through negative cost mitigation measures including water techniques for rice cultivation, agroforestry, and management of livestock diets and manure. While the MAC curve alone is insufficient to prioritize policy options, this study highlights the fundamental importance of continuous data improvement and refinement for monitoring NDC actions and ultimately achieving the goals set out in the Paris Agreement

Endothelium Derived Nitric Oxide Synthase Negatively Regulates the PDGF-Survivin Pathway during Flow-Dependent Vascular Remodeling

Chronic alterations in blood flow initiate structural changes in vessel lumen caliber to normalize shear stress. The loss of endothelial derived nitric oxide synthase (eNOS) in mice promotes abnormal flow dependent vascular remodeling, thus uncoupling mechanotransduction from adaptive vascular remodeling. However, the mechanisms of how the loss of eNOS promotes abnormal remodeling are not known. Here we show that abnormal flow-dependent remodeling in eNOS knockout mice (eNOS (−/−)) is associated with activation of the platelet derived growth factor (PDGF) signaling pathway leading to the induction of the inhibitor of apoptosis, survivin. Interfering with PDGF signaling or survivin function corrects the abnormal remodeling seen in eNOS (−/−) mice. Moreover, nitric oxide (NO) negatively regulates PDGF driven survivin expression and cellular proliferation in cultured vascular smooth muscle cells. Collectively, our data suggests that eNOS negatively regulates the PDGF-survivin axis to maintain proportional flow-dependent luminal remodeling and vascular quiescence

YY1 Regulates Melanocyte Development and Function by Cooperating with MITF

Studies of coat color mutants have greatly contributed to the discovery of genes that regulate melanocyte development and function. Here, we generated Yy1 conditional knockout mice in the melanocyte-lineage and observed profound melanocyte deficiency and premature gray hair, similar to the loss of melanocytes in human piebaldism and Waardenburg syndrome. Although YY1 is a ubiquitous transcription factor, YY1 interacts with M-MITF, the Waardenburg Syndrome IIA gene and a master transcriptional regulator of melanocytes. YY1 cooperates with M-MITF in regulating the expression of piebaldism gene KIT and multiple additional pigmentation genes. Moreover, ChIP–seq identified genome-wide YY1 targets in the melanocyte lineage. These studies mechanistically link genes implicated in human conditions of melanocyte deficiency and reveal how a ubiquitous factor (YY1) gains lineage-specific functions by co-regulating gene expression with a lineage-restricted factor (M-MITF)—a general mechanism which may confer tissue-specific gene expression in multiple lineages

Mouse hitchhiker mutants have spina bifida, dorso-ventral patterning defects and polydactyly: identification of Tulp3 as a novel negative regulator of the Sonic hedgehog pathway

The mammalian Sonic hedgehog (Shh) signalling pathway is essential for embryonic development and the patterning of multiple organs. Disruption or activation of Shh signalling leads to multiple birth defects, including holoprosencephaly, neural tube defects and polydactyly, and in adults results in tumours of the skin or central nervous system. Genetic approaches with model organisms continue to identify novel components of the pathway, including key molecules that function as positive or negative regulators of Shh signalling. Data presented here define Tulp3 as a novel negative regulator of the Shh pathway. We have identified a new mouse mutant that is a strongly hypomorphic allele of Tulp3 and which exhibits expansion of ventral markers in the caudal spinal cord, as well as neural tube defects and preaxial polydactyly, consistent with increased Shh signalling. We demonstrate that Tulp3 acts genetically downstream of Shh and Smoothened (Smo) in neural tube patterning and exhibits a genetic interaction with Gli3 in limb development. We show that Tulp3 does not appear to alter expression or processing of Gli3, and we demonstrate that transcriptional regulation of other negative regulators (Rab23, Fkbp8, Thm1, Sufu and PKA) is not affected. We discuss the possible mechanism of action of Tulp3 in Shh-mediated signalling in light of these new data

Neuromatch Academy: a 3-week, online summer school in computational neuroscience

Neuromatch Academy (https://academy.neuromatch.io; (van Viegen et al., 2021)) was designed as an online summer school to cover the basics of computational neuroscience in three weeks. The materials cover dominant and emerging computational neuroscience tools, how they complement one another, and specifically focus on how they can help us to better understand how the brain functions. An original component of the materials is its focus on modeling choices, i.e. how do we choose the right approach, how do we build models, and how can we evaluate models to determine if they provide real (meaningful) insight. This meta-modeling component of the instructional materials asks what questions can be answered by different techniques, and how to apply them meaningfully to get insight about brain function

A chromosome conformation capture ordered sequence of the barley genome

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Global, regional, and national burden of colorectal cancer and its risk factors, 1990–2019: a systematic analysis for the Global Burden of Disease Study 2019

Funding: F Carvalho and E Fernandes acknowledge support from Fundação para a Ciência e a Tecnologia, I.P. (FCT), in the scope of the project UIDP/04378/2020 and UIDB/04378/2020 of the Research Unit on Applied Molecular Biosciences UCIBIO and the project LA/P/0140/2020 of the Associate Laboratory Institute for Health and Bioeconomy i4HB; FCT/MCTES through the project UIDB/50006/2020. J Conde acknowledges the European Research Council Starting Grant (ERC-StG-2019-848325). V M Costa acknowledges the grant SFRH/BHD/110001/2015, received by Portuguese national funds through Fundação para a Ciência e Tecnologia (FCT), IP, under the Norma Transitória DL57/2016/CP1334/CT0006.proofepub_ahead_of_prin