This parody of evo devo makes it sound a lot like ID

_{Denyse O'Leary

December 19, 2017

Cell biology, Evolution, Evolutionary biology}

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“This is how we go from single cells to people.” Hmmm.

See also: From Biology Direct: Darwinism, now thoroughly detached from its historical roots as a falsifiable theory, “must be abandoned”

Comments

Sewall Wright's fitness landscape introduced the concept of evolutionary spaces in 1932. George Gaylord Simpson modified this to an adaptive, phenotypic landscape in 1944 and since then evolutionary spaces have played an important role in evolutionary theory through fitness and adaptive landscapes, phenotypic and functional trait spaces, morphospaces and related concepts. Although the topology of such spaces is highly variable, from locally Euclidean to pre-topological, evolutionary change has often been interpreted as a search through a pre-existing space of possibilities, with novelty arising by accessing previously inaccessible or difficult to reach regions of a space. Here I discuss the nature of evolutionary novelty and innovation within the context of evolutionary spaces, and argue that the primacy of search as a conceptual metaphor ignores the generation of new spaces as well as other changes that have played important evolutionary roles. This article is part of the themed issue ‘Process and pattern in innovations from cells to societies’. Erwin, Douglas. (2017). The topology of evolutionary novelty and innovation in macroevolution. Philosophical Transactions of the Royal Society B: Biological Sciences. 372. 20160422. 10.1098/rstb.2016.0422.Dionisio_{January 28, 2018
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The history of life as documented by the fossil record encompasses evolutionary diversifications at scales ranging from the Ediacaran-Cambrian explosion of animal life and the invasion of land by vascular plants, insects and vertebrates to the diversification of flowering plants over the past 100 million years and the radiation of horses. Morphological novelty and innovation has been a recurrent theme. The architects of the modern synthesis of evolutionary theory made three claims about evolutionary novelty and innovation: first, that all diversifications in the history of life represent adaptive radiations; second, that adaptive radiations are driven principally by ecological opportunity rather than by the supply of new morphological novelties, thus the primary questions about novelty and innovation focus on their ecological and evolutionary success; and third, that the rate of morphological divergence between taxa was more rapid early in the history of a clade but slowed over time as ecological opportunities declined. These claims have strongly influenced subsequent generations of evolutionary biologists, yet over the past two decades each has been challenged by data from the fossil record, by the results of comparative phylogenetic analyses and through insights from evolutionary developmental biology. Consequently a broader view of novelty and innovation is required. An outstanding issue for future work is identifying the circumstances associated with different styles of diversification and whether their frequency has changed through the history of life. Erwin, Douglas. (2015). Novelty and Innovation in the History of Life. Current Biology. 25. R930-R940. 10.1016/j.cub.2015.08.019.Dionisio_{January 28, 2018
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Since the last major theoretical integration in evolutionary biology—the modern synthesis (MS) of the 1940s—the biosciences have made significant advances. The rise of molecular biology and evolutionary developmental biology, the recognition of ecological development, niche construction and multiple inheritance systems, the ‘-omics’ revolution and the science of systems biology, among other developments, have provided a wealth of new knowledge about the factors responsible for evolutionary change. Some of these results are in agreement with the standard theory and others reveal different properties of the evolutionary process. A renewed and extended theoretical synthesis, advocated by several authors in this issue, aims to unite pertinent concepts that emerge from the novel fields with elements of the standard theory. The resulting theoretical framework differs from the latter in its core logic and predictive capacities. Whereas the MS theory and its various amendments concentrate on genetic and adaptive variation in populations, the extended framework emphasizes the role of constructive processes, ecological interactions and systems dynamics in the evolution of organismal complexity as well as its social and cultural conditions. Single-level and unilinear causation is replaced by multilevel and reciprocal causation. Among other consequences, the extended framework overcomes many of the limitations of traditional gene-centric explanation and entails a revised understanding of the role of natural selection in the evolutionary process. All these features stimulate research into new areas of evolutionary biology. Müller, Gerd. (2017). Why an extended evolutionary synthesis is necessary. Interface Focus. 7. 20170015. 10.1098/rsfs.2017.0015.Dionisio_{January 28, 2018
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The encounter in the 1960s between molecular biology and evolutionary biology had short- and long-term consequences. Comparison of protein sequences suggested that evolution proceeded at a regular pace, obeying a molecular clock. It rapidly led evolutionary biologists to give neutral variations a larger role in their models. The development of genetic engineering technologies opened the door to progressive replacement of the abstract notions of gene and gene mutation hitherto used by evolutionary biologists by precise molecular descriptions. The precise structural and functional characterization of mutations assumed an increasing role and supported the introduction of a hierarchy between genes and between gene mutations that is clearly visible in evolutionary developmental biology. I will examine how far the accumulation of molecular data has challenged the Modern Synthesis established in the 1940s. In particular, different molecular mechanisms have been successively proposed to support a Lamarckian form of evolution. My conclusion will be that molecularization of evolutionary biology is still in its infancy, and that the Modern Synthesis will be replaced by a functional synthesis in which models of evolutionary biology and a description of molecular mechanisms will be intimately dovetailed. Morange, Michel. (2017). Molecularizing Evolutionary Biology. 271-288. 10.1007/978-3-319-69123-7_12.Dionisio_{January 28, 2018
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In this paper, We study an one--dimensional morphogenesis model considered by C. Stinner et al. in (Math. Meth. Appl. Sci. 2012,35 (445-465). Under homogeneous boundary conditions, we prove the existence of nonconstant positive steady states through local bifurcation theories. We also rigorously study the stability of the nonconstant solutions when the sensitivity function are chosen to be linear and logarithmic function respectively. Finally, we present numerical solutions to illustrate the formation of stable spatially inhomogeneous patterns. Our numerical simulations suggests that this model can develop very complicated and interesting structures even over one--dimensional finite domains. Chen, Haohao & Tong, Bo & Wang, Qi. (2014). Existence and stability of nonconstant positive steady states of morphogenesis models. Mathematical Methods in the Applied Sciences. 38. . 10.1002/mma.3321.Dionisio_{January 28, 2018
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Morphogen transport is a biological process, occurring in the tissue of living organisms, which is a determining step in cell differentiation. We present rigorous analysis of a simple model of this process, which is a system coupling parabolic PDE with ODE. We prove existence and uniqueness of solutions for both stationary and evolution problems. Moreover we show that the solution converges exponentially to the equilibrium in $C^1times C^0$ topology. We prove all results for arbitrary dimension of the domain. Our results improve significantly previously known results for the same model in the case of one dimensional domain. Ma?ogrosz, Marcin. (2011). Well-posedness and asymptotic behavior a multidimensional model of morphogen transport. Journal of Evolution Equations. 12. . 10.1007/s00028-012-0135-5.Dionisio_{January 28, 2018
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We analyse a one dimensional version of a model of morphogen transport, a biological process governing cell differentiation. The model was proposed by Hufnagel et al. to describe the forming of morphogen gradient in the wing imaginal disc of the fruit fly. In mathematical terms the model is a system of reaction-diffusion equations which consists of two parabolic PDE's and three ODE's. The source of ligands is modelled by a Dirac Delta. Using semigroup approach and $L_1$ techniques we prove that the system is well-posed and possesses a unique steady state. All results are proved without imposing any artificial restrictions on the range of parameters. Ma?ogrosz, Marcin. (2012). A model of morphogen transport in the presence of glypicans I. Nonlinear Analysis: Theory, Methods & Applications. 83. . 10.1016/j.na.2012.10.012.Dionisio_{January 28, 2018
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A model of morphogen transport consisting of two evolutionary PDEs of reaction-diffusion type and three ODEs posed on a rectangular domain is analysed. We prove that the problem is globally well-posed and that the corresponding solutions converge, as the width of the rectangle tends to zero, to the unique solution of the one dimensional system which was analyzed in the first paper of the series. Main difficulties in the analysis stem from the presence of a singular source term - a Dirac Delta combined with no smoothing effect in the ODE part of the system. Ma?ogrosz, Marcin. (2014). A model of morphogen transport in the presence of glypicans II. . . . 10.1016/j.jmaa.2015.07.053.Dionisio_{January 28, 2018
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We analyse a stationary problem for the two dimensional model of morphogen transport introduced by Hufnagel et al. The model consists of one linear elliptic PDE posed on a rectangle which is coupled via a nonlinear boundary condition with a second order semilinear ODE posed on the side of the domain. The main result of the article is the existence of the unique steady state for all ranges of parameters present in the system. Moreover, we consider the problem of the dimension reduction. After introducing an appropriate scaling in the model we prove that the stationary solution converges to the unique steady state of the one-dimensional simplification of the model which was analysed in the first part of the series of papers. The main difficulty in obtaining appropriate estimates stems from the presence of a measure source term in the boundary condition. Ma?ogrosz, Marcin. (2015). A model of morphogen transport in the presence of glypicans III. Nonlinear Analysis: Real World Applications. 31. . 10.1016/j.nonrwa.2016.01.007.Dionisio_{January 28, 2018
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Morphogens are diffusive molecules produced by cells, sending signals to neighboring cells in tissues for communication. As a result, tissues develop cellular patterns that depend on the concentration levels of the morphogens. The formation of morphogen gradients is among the most fundamental biological processes during development, regeneration, and disease. During the past two decades, sophisticated mathematical models have been utilized to decipher the complex biological mechanisms that regulate the spatial and temporal dynamics of morphogens. Here, we review the model formulations for morphogen systems and present the mathematical questions and challenges that arise from the model analysis, with an emphasis on Drosophila. We discuss several important aspects of modeling frameworks: robustness, stochastic dynamics, growth control, and mechanics of morphogen-mediated patterning. Lei, Jinzhi & Lo, Wing Cheong & Nie, Qing. (2016). Mathematical models of morphogen dynamics and growth control. Annals of Mathematical Sciences and Applications. 1. 427-471. 10.4310/AMSA.2016.v1.n2.a6.Dionisio_{January 28, 2018
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Very old paper: In the development of a biological entity, ligands (such as Decapentaplegic (Dpp) along the anterior-posterior axis of the Drosophila wing imaginal disc) are synthesized at a localized source and transported away from the source for binding with cell surface receptors to form concentration gradients of ligand-receptor complexes for cell signaling. Generally speaking, activities such as diffusion and reversible binding with degradable receptors also take place in the region of ligand production. The effects of such morphogen activities in the region of localized distributed ligand source on the ligand-receptor concentration gradient in the entire biological entity have been modeled and analyzed as System F in [1]. In this paper, we deduce from System F, a related end source model (System A) in which the effects of the distributed ligand source is replaced by an idealized point stimulus at the border between the (posterior) chamber and the ligand production region that simulates the average effects of the ligand activities in the production zone. This aggregated end source model is shown to adequately reproduce the significant implications of System F and to contain the corresponding ad hoc point source model, System R of [2], as a special case. Because of its simpler mathematical structure and the absence of any limitation on the ligand synthesis rate for the existence of steady-state gradients, System A type models are expected to be used widely. An example of such application is the recent study of the inhibiting effects of the formation of nonsignaling ligand-nonreceptor complexes [3]. Lander, AD & Nie, Q & Vargas, B & Y M Wan, F. (2005). Aggregation of a Distributed Source in Morphogen Gradient Formation. SIAM journal on applied dynamical systems. 114. 343-374. 10.1111/j.0022-2526.2005.01556.x.Dionisio_{January 28, 2018
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Influenza A virus (IAV) consists of eight viral RNA (vRNA) segments that are replicated in the host cell nucleus and transported to the plasma membrane for packaging into progeny virions. We have previously proposed a model where subcomplexes of vRNA are exported from the nucleus and assembled en route to the plasma membrane. However, the role of host cytoskeletal proteins in the cytoplasmic assembly of IAV vRNA segments remains unknown. Previous studies have suggested that IAV vRNA segments are transported via Rab11A-containing recycling endosomes (RE) and use both microtubules (MT) and actin. Rab11A RE transport primarily along MT; therefore, investigation of the role of MT in vRNA assembly is warranted. We explored the role of MT in vRNA assembly and replication by using multiple IAV strains in various cell types, including primary human airway epithelial cells. We observed that Rab11A localization was altered in the presence of MTdepolymerizing drugs, but growth of IAV in all of the cell types tested was unchanged. Fluorescent in situ hybridization was performed to determine the role of MT in the assembly of multiple vRNA segments. Unexpectedly, we found that vRNAvRNA association in cytoplasmic foci was independent of MT. Given the disparity of localization between Rab11A and vRNA segments in the absence of intact MT filaments, we analyzed the three-dimensional spatial relationship between Rab11A and vRNA in the cytoplasm of infected cells. We found that Rab11A and vRNA colocalization is dependent upon dynamic MT filaments. Taken together, our data suggest that cytoplasmic transport of influenza vRNA may include a Rab11A RE-independent mechanism.
Nturibi, Eric & R. Bhagwat, Amar & Coburn, Stefanie & M. Myerburg, Mike & Lakdawala, Seema. (2017). Intracellular Colocalization of Influenza Viral RNA and Rab11A Is Dependent upon Microtubule Filaments. Journal of Virology. 91. JVI.01179-17. 10.1128/JVI.01179-17.

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Cell division-cytokinesis-involves large-scale rearrangements of the entire cell. Primarily driven by cytoskeletal proteins, cytokinesis also depends on topological rearrangements of the plasma membrane, which are coordinated with nuclear division in both space and time. Despite the fundamental nature of the process, different types of eukaryotic cells show variations in both the structural mechanisms of cytokinesis and the regulatory controls. In animal cells and fungi, a contractile actomyosin-based structure plays a central, albeit flexible, role. Here, the underlying molecular mechanisms are summarized and integrated and common themes are highlighted.
Glotzer, Michael. (2016). Cytokinesis in Metazoa and Fungi. Cold Spring Harbor perspectives in biology. 9. . 10.1101/cshperspect.a022343.

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@278 addendum
After reading recent reviews on cytokinesis (D’Avino et al., 2015; Willet et al., 2015b; Cheffings et al., 2016; Glotzer, 2016; Meitinger and Palani, 2016; Bhavsar-Jog and Bi, 2017), a new research assistant in a friend’s laboratory asked, “Because so much is known about cytokinesis, why is research on cytokinesis still important?” Although much has been learned in the past 40 yr since cell biologists reported in the Journal of Cell Biology the first molecules contributing to cytokinesis, actin filaments (Schroeder, 1972), and myosin-II (Fujiwara and Pollard, 1976; Mabuchi and Okuno, 1977), the process is so complicated that many fundamental questions remain. Nine questions, most posed 40 to 50 yr ago, remain unanswered or incompletely understood (Fig. 1).
Nine unanswered questions about cytokinesis Thomas D. Pollard J Cell Biol Aug 2017, jcb.201612068; DOI: 10.1083/jcb.201612068 http://jcb.rupress.org/content/early/2017/08/11/jcb.201612068

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Experiments on model systems have revealed that cytokinesis in cells with contractile rings (amoebas, fungi, and animals) depends on shared molecular mechanisms in spite of some differences that emerged during a billion years of divergent evolution. Understanding these fundamental mechanisms depends on identifying the participating proteins and characterizing the mechanisms that position the furrow, assemble the contractile ring, anchor the ring to the plasma membrane, trigger ring constriction, produce force to form a furrow, disassemble the ring, expand the plasma membrane in the furrow, and separate the daughter cell membranes. This review reveals that fascinating questions remain about each step. D. Pollard, Thomas. (2017). Nine unanswered questions about cytokinesis. The Journal of Cell Biology. 216. jcb.201612068. 10.1083/jcb.201612068. http://jcb.rupress.org/content/early/2017/08/11/jcb.201612068.full-text.pdfDionisio_{January 27, 2018
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Fluorescent nanodiamonds are promising probes for nanoscale magnetic resonance measurements. Their physical properties predict them to have particularly useful applications in intracellular analysis. Before using them in intracellular experiments however, it should be clear whether diamond particles influence cell biology. While cytotoxicity has already been ruled out in previous studies, we consider the non-fatal influence of fluorescent nanodiamonds on the formation of reactive oxygen species (an important stress indicator and potential target for intracellular sensing) for the first time. We investigated the influence of different sizes, shapes and concentrations of nanodiamonds on the genetic and protein level involved in oxidative stress-related pathways of the HeLa cell, an important model cell line in research. The changes in viability of the cells and the difference in intracellular levels of free radicals, after diamond uptake, are surprisingly small. At lower diamond concentrations, the cellular metabolism cannot be distinguished from that of untreated cells. This research supports the claims of non-toxicity and includes less obvious non-fatal responses. Finally, we give a handhold concerning the diamond concentration and size to use for non-toxic, intracellular measurements in favour of (cancer) research in HeLa cells. Hemelaar, Simon & Saspaanithy, Babujhi & R. M. L’Hommelet, Severin & P. Perona Martinez, Felipe & J. van der Laan, Kiran & Schirhagl, R. (2018). The Response of HeLa Cells to Fluorescent NanoDiamond Uptake. Sensors. 18. 355. 10.3390/s18020355.Dionisio_{January 27, 2018
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Cytokinesis cleaves a cell into two daughters at the end of mitosis, and must be spatially coordinated with chromosome segregation to prevent aneuploidy. The dogma is that the mitotic spindle governs the assembly and constriction of an actomyosin ring. Here, we reveal a function for active Ran in spatially restricting the ring. Our model is that during anaphase, 'free' importins, whose gradient inversely correlates with active Ran and chromatin position, function as a molecular ruler for the recruitment and localization of anillin, a contractile protein and crucial regulator of cytokinesis. We found that decreasing Ran-GTP levels, or tethering active Ran to the equatorial membrane affects anillin's localization and causes cytokinesis phenotypes. Anillin contains a conserved Nuclear Localization Signal (NLS) in its C-terminus that binds to importin-?, and is required for cortical polarity and cytokinesis. Mutating the NLS decreases anillin's cortical affinity, causing it to be more dominantly regulated by microtubules. Anillin contains a RhoA-GTP binding domain, which autoinhibits the NLS and neighbouring microtubule-binding domain, and RhoA-GTP binding may relieve this inhibition during mitosis. Retention of the C-terminal NLS in anillin homologues suggests that this is a conserved mechanism to control anillin function. Beaudet, Daniel & Akhshi, Tara & Phillipp, Julia & Law, Christopher & Piekny, Alisa. (2017). Active Ran regulates anillin function during cytokinesis. Molecular Biology of the Cell. 28. mbc.E17-04. 10.1091/mbc.E17-04-0253.Dionisio_{January 27, 2018
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@274 & @276 Very interestingDionisio_{January 27, 2018
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During cytokinesis, a contractile ring generates the constricting force to divide a cell into two daughters. This ring is composed of filamentous actin and the motor protein myosin, along with additional structural and regulatory proteins, including anillin. Anillin is a required scaffold protein that links the actomyosin ring to membrane and its organizer, RhoA. However, the molecular basis for timely action of anillin at cytokinesis remains obscure. Here, we find that phosphorylation regulates efficient recruitment of human anillin to the equatorial membrane. Anillin is highly phosphorylated in mitosis, and is a substrate for mitotic kinases. We surveyed function of 46 residues on anillin previously found to be phosphorylated in human cells to identify those required for cytokinesis. Among these sites, we identified S635 as a key site mediating cytokinesis. Preventing S635 phosphorylation adjacent to the AH domain disrupts anillin concentration at the equatorial cortex at anaphase, whereas a phosphomimetic mutant, S635D, partially restores this localization. Time-lapse videomicroscopy reveals impaired recruitment of S635A anillin to equatorial membrane and a transient unstable furrow followed by ultimate failure in cytokinesis. A phosphospecific antibody confirms phosphorylation at S635 in late cytokinesis, although it does not detect phosphorylation in early cytokinesis, possibly due to adjacent Y634 phosphorylation. Together, these findings reveal that anillin recruitment to the equatorial cortex at anaphase onset is enhanced by phosphorylation and promotes successful cytokinesis. Kim, Hyunjung & M. Johnson, James & Lera, Robert & Brahma, Sarang & E. Burkard, Mark. (2017). Anillin Phosphorylation Controls Timely Membrane Association and Successful Cytokinesis. PLOS Genetics. 13. e1006511. 10.1371/journal.pgen.1006511.Dionisio_{January 27, 2018
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The processing of amyloid precursor protein (APP) to the neurotoxic pro-aggregatory A? peptide is controlled by the mechanisms that govern the trafficking and localisation of APP. We hypothesised that genes involved in endosomal protein sorting could play an important role in regulating APP processing and, therefore, analysed ~ 40 novel endosome-to-Golgi retrieval genes previously identified in a genome-wide siRNA screen. We report that phospholipase D3 (PLD3), a type II membrane protein, functions in endosomal protein sorting and plays an important role in regulating APP processing. PLD3 co-localises with APP in endosomes and loss of PLD3 function results in reduced endosomal tubules, impaired trafficking of several membrane proteins and reduced association of sortilin-like 1 with APP. S. Mukadam, Aamir & Y. Breusegem, Sophia & Seaman, Matthew. (2018). Analysis of novel endosome-to-Golgi retrieval genes reveals a role for PLD3 in regulating endosomal protein sorting and amyloid precursor protein processing. Cellular and Molecular Life Sciences. . 10.1007/s00018-018-2752-9.Dionisio_{January 27, 2018
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Necroptosis is an alternative programmed cell death pathway that is unleashed in the absence of apoptosis and mediated by signaling complexes containing receptor-interating protein kinase 1 (RIPK1) and RIPK3. This form of cell death has recently been implicated in host defense system to eliminate pathogen-infected cells. However, only a few viral species such as herpes simplex virus (HSV) and cytomegalovirus (CMV) have evolved mechanisms inhibiting necroptosis to overcome host antiviral defense, which is important for successful pathogenesis. Here, we show that the ?-herpesvirus Epstein–Barr virus (EBV) blocks necroptosis in EBV-infected human nasopharyngeal epithelial cells and nasopharyngeal carcinoma cells. Our findings indicate that EBV-encoded latent membrane protein 1 (LMP1), which lacks an RIP homotypic interaction motif (RHIM) domain, has mechanisms distinct from RHIM signaling competition to inhibit this necroptotic pathway. Intriguingly, LMP1 interacts directly with both RIPK1 and RIPK3 through its C-terminal activation region. More importantly, LMP1 can modulate the post-translational modification of the two receptor-interacting proteins. We then show that LMP1-mediated promotion of K63-polyubiquitinated RIPK1, suppression of RIPK1 protein expression and inhibition of K63-polyubiquitinated RIPK3 induced a switch in cell fate from necroptotic death to survival. These findings provide direct evidence for the suppression of necroptosis by EBV and define a mechanism of LMP1 to interrupt the initiation process of necroptosis before necrosome formation. Liu, Xiaolan & Li, Yueshuo & Peng, Songling & yu, Xinfang & Li, Wei & Shi, Feng & Luo, Xiangjian & Tang, Min & Tan, Zheqiong & Bode, Ann & Cao, Ya. (2018). Epstein-Barr virus encoded latent membrane protein 1 suppresses necroptosis through targeting RIPK1/3 ubiquitination. Cell Death & Disease. 9. 53. 10.1038/s41419-017-0081-9.Dionisio_{January 27, 2018
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Acute respiratory distress syndrome (ARDS) is the leading cause of death in critical care medicine. The syndrome is typified by an exaggerated inflammatory response within the lungs. ARDS has been reported in many species, including dogs. We have previously reported a fatal familial juvenile respiratory disease accompanied by occasional unilateral renal aplasia and hydrocephalus, in Dalmatian dogs. The condition with a suggested recessive mode of inheritance resembles acute exacerbation of usual interstitial pneumonia in man. We combined SNP-based homozygosity mapping of two ARDS-affected Dalmatian dogs and whole genome sequencing of one affected dog to identify a case-specific homozygous nonsense variant, c.31C>T; p.R11* in the ANLN gene. Subsequent analysis of the variant in a total cohort of 188 Dalmatians, including seven cases, indicated complete segregation of the variant with the disease and confirmed an autosomal recessive mode of inheritance. Low carrier frequency of 1.7% was observed in a population cohort. The early nonsense variant results in a nearly complete truncation of the ANLN protein and immunohistochemical analysis of the affected lung tissue demonstrated the lack of the membranous and cytoplasmic staining of ANLN protein in the metaplastic bronchial epithelium. The ANLN gene encodes an anillin actin binding protein with a suggested regulatory role in the integrity of intercellular junctions. Our study suggests that defective ANLN results in abnormal cellular organization of the bronchiolar epithelium, which in turn predisposes to acute respiratory distress. ANLN has been previously linked to a dominant focal segmental glomerulosclerosis in human without pulmonary defects. However, the lack of similar renal manifestations in the affected Dalmatians suggest a novel ANLN-related pulmonary function and disease association. Holopainen, Saila & Hytönen, Marjo & Syrja, Pernilla & Arumilli, Meharji & Järvinen, Anna-Kaisa & Rajamäki, Minna & Lohi, Hannes. (2017). ANLN truncation causes a familial fatal acute respiratory distress syndrome in Dalmatian dogs. PLoS genetics. 13. e1006625. 10.1371/journal.pgen.1006625.Dionisio_{January 27, 2018
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The anaphase spindle determines the position of the cytokinesis furrow, such that the contractile ring assembles in an equatorial zone between the two spindle poles. Contractile ring formation is mediated by RhoA activation at the equator by the centralspindlin complex and midzone microtubules. Astral microtubules also inhibit RhoA accumulation at the poles. In the C. elegans one-cell embryo, the astral microtubule dependent pathway requires anillin, NOP-1 and LET-99. LET-99 is well characterized for generating the asymmetric cortical localization of the G?-dependent force-generating complex that positions the spindle during asymmetric division. However, whether LET-99's role in cytokinesis is specific to asymmetric division, and whether it acts through G? to promote furrowing is unclear. Here we show that LET-99 localizes to the equator in the symmetrically dividing AB cell where it is required for astral microtubule dependent furrowing, but G? is not needed. LET-99 acts in a pathway parallel to anillin and is required for myosin enrichment into the contractile ring. These and other results suggest a feedback model in which LET-99 localizes to the presumptive cleavage furrow in response to the spindle and myosin. Once positioned there, LET-99 enhances myosin accumulation to promote furrowing in both symmetrically and asymmetrically dividing cells. L. Price, Kari & S. Rose, Lesilee. (2017). LET-99 functions in the astral furrowing pathway where it is required for myosin enrichment in the contractile ring. Molecular Biology of the Cell. 28. mbc.E16-12. 10.1091/mbc.E16-12-0874.Dionisio_{January 27, 2018
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During female meiosis, haploid eggs are generated from diploid oocytes. This reduction in chromosome number occurs through two highly asymmetric cell divisions resulting in one large egg and two small polar bodies. Unlike mitosis, where an actomyosin contractile ring forms between the sets of segregating chromosomes, the meiotic contractile ring forms on the cortex adjacent to one spindle pole, then ingresses down the length of the spindle to position itself at the exact midpoint between the two sets of segregating chromosomes. Depletion of casein kinase 1 gamma (CSNK-1) in C. elegans led to the formation of large polar bodies that contain all maternal DNA because the contractile ring ingressed past the spindle midpoint. Depletion of CSNK-1 also resulted in the formation of deep membrane invaginations during meiosis, suggesting an effect on cortical myosin. Both myosin and anillin assemble into dynamic rho-dependent cortical patches that rapidly disassemble in wild-type embryos. CSNK-1 was required for disassembly of both myosin patches and anillin patches. Disassembly of anillin patches was myosin independent suggesting that CSNK-1 prevents expulsion of the entire meiotic spindle into a polar body by negatively regulating the rho pathway rather than through direct inhibition of myosin. Flynn, Jonathan & J. McNally, Francis. (2017). A Casein Kinase 1 Prevents Expulsion of the Oocyte Meiotic Spindle into a Polar Body by Regulating Cortical Contractility. Molecular Biology of the Cell. 28. mbc.E17-01. 10.1091/mbc.E17-01-0056.Dionisio_{January 27, 2018
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@267 addendum Van Arsdale, Adam. (2017). Human Evolution as a Theoretical Model for an Extended Evolutionary Synthesis. 105-130. 10.1007/978-3-319-69123-7_6.Dionisio_{January 27, 2018
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Humans have occupied a paradoxical position within the history of evolutionary studies. On one end, humans have been central to both the academic motivation of the field and the public tensions surrounding evolution. Simultaneously, humans have been cast aside as a poor model organism for understanding the processes that underlie evolutionary theory. As a result, anthropologists who work within an evolutionary context, often chided as being two decades behind mainstream biology, have come to occupy a unique position with respect to the understanding of how evolution operates on humans. Incorporating theoretical developments from a diverse set of related evolutionary fields, biological anthropologists have begun to gather empirical data on the unique evolutionary processes that have shaped our own evolutionary path. Some of the important components that have emerged in human evolutionary studies—biocultural feedback systems, culturally mediated niche construction, and technological ratchet effects—have shed new light not only on how human evolution has proceeded but also on the range of capabilities of evolution more broadly. While not rejecting traditional neo-Darwinian theory and the importance of genetic inheritance, these new developments have highlighted the tremendous complexity afforded by the cumulative action of both selective and neutral evolutionary forces across a range of inheritance modes. Rather than a poor evolutionary model, many of these evolutionary processes are best, or perhaps only, observable in humans. The traits which have structured critical transitions in our hominin past—encephalization, expanded childhood development, and generative language—open up new windows into thinking about an Extended Evolutionary Synthesis. Where's the beef?Dionisio_{January 27, 2018
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Zinc is a metal ion that is an essential cell signaling molecule. Highlighting this, zinc is an insulin mimetic, activating cellular pathways that regulate cellular homeostasis and physiological responses. Previous studies have linked dysfunctional zinc signaling with several disease states including cancer, obesity, cardiovascular disease and type 2 diabetes. The present study evaluated the insulin-like effects of zinc on cell signaling molecules including tyrosine, PRSA40, Akt, ERK1/2, SHP-2, GSK-3? and p38, and glucose oxidation in human and mouse skeletal muscle cells. Insulin and zinc independently led to the phosphorylation of these proteins over a 60-minute time course in both mouse and human skeletal muscle cells. Similarly, utilizing a protein array we identified that zinc could active the phosphorylation of p38, ERK1/2 and GSK-3B in human and ERK1/2 and GSK-3B in mouse skeletal muscle cells. Glucose oxidation assays were performed on skeletal muscle cells treated with insulin, zinc, or a combination of both and resulted in a significant induction of glucose consumption in mouse (p<0.01) and human (p<0.05) skeletal muscle cells when treated with zinc alone. Insulin, as expected, increased glucose oxidation in mouse (p<0.001) and human (0.001) skeletal muscle cells, however the combination of zinc and insulin did not augment glucose consumption in these cells. Zinc acts as an insulin mimetic, activating key molecules implicated in cell signaling to maintain glucose homeostasis in mouse and human skeletal muscle cells. Zinc is an important metal ion implicated in several biological processes. The role of zinc as an insulin memetic in activating key signaling molecules involved in glucose homeostasis could provide opportunities to utilize this ion therapeutically in treating disorders associated with dysfunctional zinc signaling. (2018). Zinc stimulates glucose oxidation and glycemic control by modulating the insulin signaling pathway in human and mouse skeletal muscle cell lines. PLOS ONE. 13. e0191727. 10.1371/journal.pone.0191727.Dionisio_{January 26, 2018
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@264: More questions than answers? What else is new?Dionisio_{January 26, 2018
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Human cardiac muscle cells are the most physically energetic cells in the body, and according to various researchers they contain two nuclei in 25–40%. In humans, the heart during prenatal development consists mainly of cardiomyocytes with one nucleus. Just before birth, binucleation begins and can extend into early neonatal life. The physiological importance of binucleation is still poorly understood. In this critical review, we provide a summary of the latest research on binucleation of cardiac muscle cells, with special emphasis on the potential application of such knowledge to the fields of regenerative medicine. We summed up and discussed about ten possible biological arguments why binucleation may be beneficial for cardiac muscle cells as well as for the whole myocardium. These arguments include increase of gene expression, purposeful cell shaping, increase of metabolic activity, energy-saving growth and function, need for organ growth despite of telomere depletion, adaptation to stress (tissue regeneration), prevention of overgrowth – organ shaping, prevention of aneuploidy, terminally differentiated state (cardiomyocytes exit the cell cycle, end of proliferation activity); or, we hypothesize, binucleation is just an unwanted side product. Miko, Michal & Kyselovic, Jan & Danišovi?, ?uboš & Barczi, Tomas & Polak, Stefan & Varga, Ivan. (2017). Two nuclei inside a single cardiac muscle cell. More questions than answers about the binucleation of cardiomyocytes. Biologia. 72. . 10.1515/biolog-2017-0107.Dionisio_{January 26, 2018
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Stable cytoplasmic bridges arise from failed cytokinesis, the last step of cell division, and are a key feature of syncytial architectures in the germ line of most metazoans. Whereas the C. elegans germ line is syncytial, its formation remains poorly understood. We found that the germline precursor blastomere, P4, fails cytokinesis, leaving a stable cytoplasmic bridge between the two daughter cells, Z2 and Z3 Depletion of several regulators of actomyosin contractility resulted in a regression of the membrane partition between Z2 and Z3, indicating that they are required to stabilize the cytoplasmic bridge. Epistatic analysis revealed a pathway in which Rho regulators promote accumulation of the non-cannonical anillin ANI-2 at the stable cytoplasmic bridge, which in turns promotes the accumulation of the non-muscle myosin II NMY-2 and the midbody component CYK-7 at the bridge, in part by limiting the accumulation of canonical anillin ANI-1. Our results uncover key steps in C. elegans germline formation and define a set of conserved regulators that are enriched at the primordial germ cell cytoplasmic bridge to ensure its stability during embryonic development. Goupil, Eugénie & Amini, Rana & H. Hall, David & Labbé, Jean-Claude. (2017). Actomyosin contractility regulators stabilize the cytoplasmic bridge between the two primordial germ cells during C. elegans embryogenesis. Molecular Biology of the Cell. 28. mbc.E17-08. 10.1091/mbc.E17-08-0502.Dionisio_{January 26, 2018
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