Mystery at the heart of life

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December 21, 2014

Cell biology, Intelligent Design, News

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Cell biology
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By Biologic Institute’s Ann Gauger, at Christianity Today’s Behemoth, the secret life of cells:

Our bodies are made up of some 100 trillion cells. We tend to think of cells as static, because that’s how they were presented to us in textbooks. In fact, the cell is like the most antic, madcap, crowded (yet fantastically efficient) city you can picture. And at its heart lies a mystery—or I should say, several mysteries—involving three special kinds of molecules: DNA, RNA, and proteins.

These molecules are assembled into long chains called polymers, and are uniquely suited for the roles they play. More importantly, life absolutely depends upon them. We have to have DNA, RNA, and protein all present and active at the same time for a living organism to live.

How they work together so optimally and efficiently is not merely amazing, but also a great enigma, a mystery that lies at the heart of life itself. More. Paywall soon after. May be worth it.

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CNS myelination requires cytoplasmic dynein function DOI: 10.1002/dvdy.24238 Cytoplasmic dynein provides the main motor force for minus-end-directed transport of cargo on microtubules. Within the vertebrate central nervous system (CNS), proliferation, neuronal migration, and retrograde axon transport are among the cellular functions known to require dynein. Oligodendrocytes, the myelinating glial cell type of the CNS, migrate from their origins to their target axons and subsequently extend multiple long processes that ensheath axons with specialized insulating membrane. These processes are filled with microtubules, which facilitate molecular transport of myelin components. However, whether oligodendrocytes require cytoplasmic dynein to ensheath axons with myelin is not known. We identified a mutation of zebrafish dync1h1 in a forward genetic screen that caused a deficit of oligodendrocytes. Using in vivo imaging and gene expression analyses, we additionally found evidence that dync1h1 promotes axon ensheathment and myelin gene expression. In addition to its well known roles in axon transport and neuronal migration, cytoplasmic dynein contributes to neural development by promoting myelination. Developmental Dynamics, 2015. © 2014 Wiley Periodicals, Inc. http://onlinelibrary.wiley.com/doi/10.1002/dvdy.24238/abstract
For the above highlighted text, explain 'how' in details, by indicating the paper(s) where they answer such questions.Dionisio_{January 24, 2015
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Molecular Determinants of ?-Synuclein Mutants’ Oligomerization and Membrane Interactions ACS Chem. Neurosci., Article ASAP DOI: 10.1021/cn500332w Publication Date (Web): January 5, 2015 Copyright © 2015 American Chemical Society http://pubs.acs.org/doi/abs/10.1021/cn500332w Parkinson’s disease (PD) is associated with the formation of toxic ?-synuclein oligomers that can penetrate the cell membrane. Familial forms of PD are caused by the point mutations A53T, A30P, E46K, and H50Q. Artificial point mutations E35K and E57K also increase oligomerization and pore formation. We generated structural conformations of ?-synuclein and the above-mentioned mutants using molecular dynamics. We elucidated four main regions in these conformers contacting the membrane and found that the region including residues 39–45 (Zone2) may have maximum membrane penetration. E57K mutant had the highest rate of interaction with the membrane, followed by A53T, E46K, and E35K mutants and wild type (wt) ?-synuclein. The mutant A30P had the smallest percentage of conformers that contact the membrane by Zone 2 than all other mutants and wt ?-synuclein. These results were confirmed experimentally in vitro. We identified the key amino acids that can interact with the membrane (Y38, E62, and N65 (first hydrophilic layer); E104, E105, and D115 (second hydrophilic layer), and V15 and V26 (central hydrophobic layer)) and the residues that are involved in the interprotein contacts (L38, V48, V49, Q62, and T64). Understanding the molecular interactions of ?-synuclein mutants is important for the design of compounds blocking the formation of toxic oligomers.
How many details have to work right in the biological systems in order for the systems to function properly ?Dionisio_{January 22, 2015
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Tethering Sister Centromeres to Each Other Suggests the Spindle Checkpoint Detects Stretch within the Kinetochore •DOI: 10.1371/journal.pgen.1004492 The spindle checkpoint ensures that newly born cells receive one copy of each chromosome by preventing chromosomes from segregating until they are all correctly attached to the spindle. The checkpoint monitors tension to distinguish between correctly aligned chromosomes and those with both sisters attached to the same spindle pole. Tension arises when sister kinetochores attach to and are pulled toward opposite poles, stretching the chromatin around centromeres and elongating kinetochores. We distinguished between two hypotheses for where the checkpoint monitors tension: -between the kinetochores, by detecting alterations in the distance between them, or -by responding to changes in the structure of the kinetochore itself. To distinguish these models, we inhibited chromatin stretch by tethering sister chromatids together by binding a tetrameric form of the Lac repressor to arrays of the Lac operator located on either side of a centromere. Inhibiting chromatin stretch did not activate the spindle checkpoint; [why?] these cells entered anaphase at the same time as control cells that express a dimeric version of the Lac repressor, which cannot cross link chromatids, and cells whose checkpoint has been inactivated. There is no dominant checkpoint inhibition when sister kinetochores are held together: cells expressing the tetrameric Lac repressor still arrest in response to microtubule-depolymerizing drugs. Tethering chromatids together does not disrupt kinetochore function; [why?] chromosomes are successfully segregated to opposite poles of the spindle. Our results indicate that the spindle checkpoint does not monitor inter-kinetochore separation, thus supporting the hypothesis that tension is measured within the kinetochore. [how?] http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1004492
Dionisio_{January 21, 2015
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Evolution leading to a potential revolution? https://uncommondescent.com/evolution/a-third-way-of-evolution/#comment-543230 :)Dionisio_{January 21, 2015
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TRAIP is a regulator of the spindle assembly checkpoint doi: 10.1242/?jcs.152579 Accurate chromosome segregation during mitosis is temporally and spatially coordinated by fidelity-monitoring checkpoint systems. Deficiencies in these checkpoint systems can lead to chromosome segregation errors and aneuploidy,... the TRAF-interacting protein (TRAIP), a ubiquitously expressed nucleolar E3 ubiquitin ligase important for cellular proliferation, is localized close to mitotic chromosomes. [why is it there?] TRAIP regulates the spindle assembly checkpoint, MAD2 abundance at kinetochores and the accurate cellular distribution of chromosomes. [how does it do all that?] The TRAIP ubiquitin ligase activity is functionally required for the spindle assembly checkpoint control. http://jcs.biologists.org/content/127/24/5149.short
What mechanisms determine that a protein is ubiquitously expressed? Branch out on this expression subtopic. What determines the localization of TRAIP? Branch out on this protein localization subtopic. Search the answers within the payer first, then in other papers.Dionisio_{January 20, 2015
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Computational analysis of signaling patterns in single cells doi:10.1016/j.semcdb.2014.09.015 Signaling proteins are flexible in both form and function. They can bind to multiple molecular partners and integrate diverse types of cellular information. When imaged by time-lapse microscopy, many signaling proteins show complex patterns of activity or localization that vary from cell to cell. This heterogeneity is so prevalent that it has spurred the development of new computational strategies to analyze single-cell signaling patterns. A collective observation from these analyses is that cells appear less heterogeneous when their responses are normalized to, or synchronized with, other single-cell measurements. In many cases, these transformed signaling patterns show distinct dynamical trends that correspond with predictable phenotypic outcomes. When signaling mechanisms are unclear, computational models can suggest putative molecular interactions that are experimentally testable. Thus, computational analysis of single-cell signaling has not only provided new ways to quantify the responses of individual cells, but has helped resolve longstanding questions surrounding many well-studied human signaling proteins including NF-?B, p53, ERK1/2, and CDK2. A number of specific challenges lie ahead for single-cell analysis such as quantifying the contribution of non-cell autonomous signaling as well as the characterization of protein signaling dynamics in vivo. http://www.sciencedirect.com/science/article/pii/S1084952114002705
Dionisio_{January 20, 2015
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The centrosome orientation checkpoint is germline stem cell specific and operates prior to the spindle assembly checkpoint http://www.ncbi.nlm.nih.gov/pubmed/25480919 Asymmetric cell division is utilized by a broad range of cell types to generate two daughter cells with distinct cell fates. In stem cell populations asymmetric cell division is believed to be crucial for maintaining tissue homeostasis, failure of which can lead to tissue degeneration or hyperplasia/tumorigenesis. Asymmetric cell divisions also underlie cell fate diversification during development. Accordingly, the mechanisms by which asymmetric cell division is achieved have been extensively studied, although the check points that are in place to protect against potential perturbation of the process are poorly understood. This study may provide a framework for identifying and understanding similar mechanisms that might be in place in other asymmetrically dividing cell types.Dionisio_{January 19, 2015
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Bifurcation analysis of single-cell gene expression data reveals epigenetic landscape doi: 10.1073/pnas.1408993111 http://intl.pnas.org/content/111/52/E5643.fullDionisio_{January 19, 2015
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From Single-Cell Noise to Transcriptional Music Although an orchestra warming up before a performance may produce a meaningless mixture of sounds, the individual musicians are probably playing bits and pieces from the same score. If only listeners could isolate the fragmentary themes and motifs, and move them backwards and forwards in the imagination, order would emerge from chaos, the sense of musical arrangements would become clear. Something like this organizational power has been needed in single-cell genomics. Although individual cells all play from the same score—the genome—they don’t necessarily act as though they are following a conductor’s baton. Even cells of the same type may appear to be transcriptionally distinct simply because they are at different stages of the cell cycle, or are different ages. Confounding factors such as these can obscure deep commonalities or—to return to the orchestra analogy—unheard harmonies. http://www.genengnews.com/gen-news-highlights/from-single-cell-noise-to-transcriptional-music/81250824/Dionisio_{January 19, 2015
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The spindle checkpoint and chromosome segregation in meiosis DOI: 10.1111/febs.13166 The spindle checkpoint is a key regulator of chromosome segregation in mitosis and meiosis. Its function is to prevent precocious anaphase onset before chromosomes have achieved bipolar attachment to the spindle. The spindle checkpoint comprises a complex set of signaling pathways that integrate microtubule dynamics, biomechanical forces at the kinetochores, and intricate regulation of protein interactions and post-translational modifications. Historically, many key observations that gave rise to the initial concepts of the spindle checkpoint were made in meiotic systems. In contrast with mitosis, the two distinct chromosome segregation events of meiosis present a special challenge for the regulation of checkpoint signaling. Preservation of fidelity in chromosome segregation in meiosis, controlled by the spindle checkpoint, also has a significant impact in human health. This review highlights the contributions from meiotic systems in understanding the spindle checkpoint as well as the role of checkpoint signaling in controlling the complex divisions of meiosis. http://onlinelibrary.wiley.com/doi/10.1111/febs.13166/full
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Lentivirus?mediated silencing of spindle and kinetochore?associated protein 1 doi: 10.3892/mmr.2015.3175 Spindle and kinetochore?associated protein 1 (SKA1) is an important component of the human kinetochore, which plays a key role in mitosis. http://www.ncbi.nlm.nih.gov/pubmed/25573192Dionisio_{January 18, 2015
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Regulation of RNA granule dynamics... DOI: http://dx.doi.org/10.7554/eLife.04591 RNA granules have been likened to liquid droplets whose dynamics depend on the controlled dissolution and condensation of internal components. The molecules and reactions that drive these dynamics in vivo are not well understood. http://elifesciences.org/content/3/e04591Dionisio_{January 17, 2015
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Directed targeting of chromatin to the nuclear lamina is mediated by chromatin state and A-type lamina doi: 10.1083/jcb.201405110 Nuclear organization has been implicated in regulating gene activity. Recently, large developmentally regulated regions of the genome dynamically associated with the nuclear lamina have been identified. [...]how these lamina-associated domains (LADs) are directed to the nuclear lamina. [?] http://jcb.rupress.org/content/208/1/33
Dionisio_{January 17, 2015
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Dionisio I appreciate the paper that you provided, which linked to the open access Moser intelligence laboratory paper that was published just in time for Christmas. With my day job and all else I didn't have time to keep up with their progress. Now I just need to figure out the details, which is sure not easy for a paper like this one. And I honestly doubt for something like this I'll find much help from UD, Biologic or Discovery Institute.Gary S. Gaulin_{January 16, 2015
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Genome resilience and prevalence of segmental duplications following fast neutron irradiation of soybean doi: 10.1534/genetics.114.170340 http://www.ncbi.nlm.nih.gov/pubmed/25213171 Explain the details describing that resilience. Does the paper contain ALL the details? ALL? This means that no potential questions have been left unanswered?Dionisio_{January 16, 2015
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#153 Gary S. Gatlin Thank you for sharing the reference to that interesting paper.Dionisio_{January 16, 2015
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Mechanism of suppression of chromosomal instability by DNA polymerase POLQ. doi: 10.1371/journal.pgen.1004654 Although a defect in the DNA polymerase POLQ leads to ionizing radiation sensitivity in mammalian cells, the relevant enzymatic pathway has not been identified. Here we define the specific mechanism by which POLQ restricts harmful DNA instability. This work clearly defines a role and mechanism for mammalian POLQ in an alternative end joining pathway that suppresses the formation of chromosomal translocations. Our findings depart from the prevailing view that alternative end joining processes are generically translocation-prone. http://www.ncbi.nlm.nih.gov/pubmed/25275444Dionisio_{January 16, 2015
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Dionisio, this slightly more recent paper for the development of spatial representation is also excellent: Coherence among Head Direction Cells before Eye Opening in Rat Pups. Bjerknes TL, Langston RF, Kruge IU, Moser EI, Moser MB.
Abstract Mammalian navigation is thought to depend on an internal map of space consisting of functionally specialized cells in the hippocampus and the surrounding parahippocampal cortices [1-7]. Basic properties of this map are present when rat pups explore the world outside of their nest for the first time, around postnatal day 16-18 (P16-P18) [8-10]. One of the first functions to be expressed in navigating animals is the directional tuning of the head direction cells [8, 9]. To determine whether head direction tuning is expressed at even earlier ages, before the start of exploration, and to establish whether vision is necessary for the development of directional tuning, we recorded neural activity in pre- and parasubiculum, or medial entorhinal cortex, from P11 onward, 3-4 days before the eyelids unseal. Head direction cells were present from the first day of recording. Firing rates were lower than in adults, and preferred firing directions were less stable, drifting within trials and changing completely between trials. Yet the cells drifted coherently, i.e., relative firing directions were maintained from one trial to the next. Directional tuning stabilized shortly after eye opening. The data point to a hardwired attractor network for representation of head direction in which directional tuning develops before vision and visual input serves primarily to anchor firing direction to the external world.
doi: 10.1016/j.cub.2014.11.009. Epub 2014 Nov 26. http://www.ncbi.nlm.nih.gov/pubmed/25466682 The bolded information at the end of its abstract is vital to the further development of the Grid Cell Attractor Network and earlier model that Edvard Moser knows about. The new paper seems to have been worded so that someone like myself would immediately recognize its significance, and know how to make it work in a computer model.Gary S. Gaulin_{January 15, 2015
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Know Your Limits: The Role of Boundaries in the Development of Spatial Representation DOI: http://dx.doi.org/10.1016/j.neuron.2014.03.017 http://www.cell.com/neuron/abstract/S0896-6273(14)00247-5Dionisio_{January 15, 2015
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The mitotic checkpoint protein kinase BUB1 is an engine in the TGF-? signaling apparatus DOI: 10.1126/scisignal.aaa4636 The mitotic checkpoint guarantees faithful chromosomal segregation during cell division. ...the mitotic checkpoint kinase BUB1 promotes the activity of TGF-? receptors, which adds new molecular links between these fundamental biological processes. http://stke.sciencemag.org/content/8/359/fs1.abstract?sid=34d79839-f769-47bf-a41d-52de0b10bfc9Dionisio_{January 13, 2015
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Dom34 Rescues Ribosomes in 3? Untranslated Regions "As far as we know, this 'scanning' activity has never been seen before -- it was a big surprise." -Nick Guydosh, Ph.D. DOI: http://dx.doi.org/10.1016/j.cell.2014.02.006 Ribosomes that stall before completing peptide synthesis must be recycled and returned to the cytoplasmic pool. The protein Dom34 and cofactors Hbs1 and Rli1 can dissociate stalled ribosomes in vitro, but the identity of targets in the cell is unknown. Here, we extend ribosome profiling methodology to reveal a high-resolution molecular characterization of Dom34 function in vivo. Dom34 removes stalled ribosomes from truncated mRNAs, but, in contrast, does not generally dissociate ribosomes on coding sequences known to trigger stalling, such as polyproline. We also show that Dom34 targets arrested ribosomes near the ends of 3? UTRs. These ribosomes appear to gain access to the 3? UTR via a mechanism that does not require decoding of the mRNA. These results suggest that ribosomes frequently enter downstream noncoding regions and that Dom34 carries out the important task of rescuing them. http://www.cell.com/abstract/S0092-8674%2814%2900162-7
Dionisio_{January 13, 2015
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A unified vision of the building blocks of life? doi:10.1038/ncb0908-1015 From the discovery of DNA to the sequencing of the human genome, the template-dependent formation of biological molecules from gene to RNA and protein has been the central tenet of biology. Yet the origins of many diseases, including allergy, Alzheimer's disease, asthma, autism, diabetes, inflammatory bowel disease, Lou Gehrig's disease, multiple sclerosis, Parkinson's disease and rheumatoid arthritis, continue to evade our understanding. http://www.nature.com/ncb/journal/v10/n9/full/ncb0908-1015.htmlDionisio_{January 13, 2015
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Bleb-driven chemotaxis of Dictyostelium cells doi: 10.1083/jcb.201306147 http://jcb.rupress.org/content/204/6/1027 Dictyostelium uses ether?linked inositol phospholipids for intracellular signaling DOI 10.15252/embj.201488677 http://emboj.embopress.org/content/33/19/2188.abstract How blebs and pseudopods cooperate during chemotaxis doi: 10.1073/pnas.1322291111 http://www.pnas.org/content/111/32/11703.abstractDionisio_{January 13, 2015
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Ok, that's cool, thanks. But how did it all start? :) http://phys.org/news/2015-01-affirms-sexual-reproduction-mutations.html#nRlv Where is the beef?Dionisio_{January 13, 2015
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Researchers have looked at a species of fish to help unravel one of the biggest mysteries in evolutionary biology. "The importance of this work lies in the fundamental question: how and why do variants of the same animal exist in nature," he said. "Colour variants of the same species are a striking example of biological variation, yet the adaptive significance and what evolutionary processes maintain them, remains unknown." "Given the complexities of colour variants in species, more work is needed to understand how differences in colouration might influence the susceptibility of dark and gold individuals to different predators and under different environmental conditions," Read more at: http://phys.org/news/2015-01-devil.html#jCp How do the associated mechanisms function? what effect do they have? Check the given paper or other papers for more details Where is the beef?Dionisio_{January 13, 2015
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Morphology-based taxonomies do not accurately reflect genealogical relationships of rock sponges http://phys.org/news/2015-01-morphology-based-taxonomies-accurately-genealogical-relationships.html#nRlv Deceptive Desmas: Molecular Phylogenetics Suggests a New Classification and Uncovers Convergent Evolution of Lithistid Demosponges •DOI: 10.1371/journal.pone.0116038 http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0116038Dionisio_{January 13, 2015
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Evidence that disproves a long-standing assumption? A Singapore-based research team has used fluorescent labeling of embryonic cell populations to pinpoint the origin of scales and fins in modern-day fish. These tissues [...] were widely assumed to originate from an embryonic cell population known as the 'trunk neural crest'. Now, research led by Tom Carney of the A*STAR Institute of Molecular and Cell Biology has shown that scales and fins actually develop from a cell population called the mesoderm. Read more at: http://phys.org/news/2013-08-evidence-long-standing-assumption-fish-insight.html#jCp
What went wrong with their previous wide assumptions?Dionisio_{January 13, 2015
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New insight on skull development For more than a century, scientists have attempted to understand how the bones of the skull develop in vertebrate embryos. Most have concluded that a single developmental pattern—first described in chickens—applies to all vertebrates. A new study conducted by Harvard researchers suggests that this may not be entirely true. Read more at: http://phys.org/news/2015-01-insight-skull-frogs.html#jCp
Old consensus broken? :) How come? what went wrong in their previous thinking?Dionisio_{January 13, 2015
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mysterious molecular mechanism powering cells A team led by structural biologists at The Scripps Research Institute (TSRI) has taken a big step toward understanding the intricate molecular mechanism of a metabolic enzyme produced in most forms of life on Earth. Read more at: http://phys.org/news/2015-01-scientists-illuminate-mysterious-molecular-mechanism.html#jCpDionisio_{January 13, 2015
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Tumour-blocking role found for cell regulation molecule Manchester scientists have explored the role of a protein in regulating tumour development and found that it suppresses liver cancer growth in the lab. Read more at: http://phys.org/news/2015-01-tumour-blocking-role-cell-molecule.html#jCp JNK Suppresses Tumor Formation via a Gene-Expression Program Mediated by ATF2 DOI: http://dx.doi.org/10.1016/j.celrep.2014.10.043 http://www.cell.com/cell-reports/abstract/S2211-1247(14)00912-7?_returnURL=http%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS2211124714009127%3Fshowall%3DtrueDionisio_{January 13, 2015
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