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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Comments

In the developing central nervous system, most neurogenesis occurs in the ventricular and subventricular proliferative zones. It is essential that an organ and its blood supply should develop together in synchrony to allow optimal conditions for the different stages of growth, differentiation and changing functional requirements. Both the CSF and the vasculature of the brain provide regulatory niches for neurogenesis in the developing and adult brain. The localization of neurogenic niches makes them sensitive to circulating soluble factors. The local and systemic control of the neurogenic niches therefore has significant impact on brain function throughout life. [...] it is essential that we increase our understanding of the control of neurogenic niches [...]
Neurogenic niches in the brain: help and hindrance of the barrier systems Helen B. Stolp1,* and Zoltán Molnár Front Neurosci. 9: 20. doi: 10.3389/fnins.2015.00020

Dionisio_{July 21, 2016
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[...] we have identified an important role of Alix in preserving the characteristics and functionality of an apical TJ complex responsible for epithelial cell polarity. Alix exerts these functions by securing the correct positioning and interactions of junctional proteins within a macromolecular assembly with the actomyosin cytoskeleton [...] These findings add a tier to the regulation of junctional complexes in the epithelium that extend beyond the CP and the ependymal [...] It is tempting to speculate that the diverse functions of Alix may be primarily related to the capacity of this scaffold protein to directly interact with the actin cytroskeleton, thereby creating the most favourable setting for components of multiprotein complexes to assemble in a timely, spatial and dynamic manner and to target them to specific cellular microdomains.
Alix-mediated assembly of the actomyosin–tight junction polarity complex preserves epithelial polarity and epithelial barrier Yvan Campos,1 Xiaohui Qiu,1 Elida Gomero,1 Randall Wakefield,2 Linda Horner,2 Wojciech Brutkowski,3 Young-Goo Han,4 David Solecki,4 Sharon Frase,2 Antonella Bongiovanni,5 and Alessandra d’Azzo Nat Commun. 7: 11876. doi: 10.1038/ncomms11876

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[...] by interacting with F-actin, the Par complex and ZO-1, Alix ensures the formation and maintenance of the apically restricted actomyosin–tight junction complex. [...] in this capacity Alix plays a role in the establishment of apical–basal polarity and in the maintenance of the epithelial barrier. [...] the molecular signals that regulates the connection between different TJ complexes and the actomyosin network to support a functional epithelial barrier are still poorly understood in a mammalian system [...]
Alix-mediated assembly of the actomyosin–tight junction polarity complex preserves epithelial polarity and epithelial barrier Yvan Campos,1 Xiaohui Qiu,1 Elida Gomero,1 Randall Wakefield,2 Linda Horner,2 Wojciech Brutkowski,3 Young-Goo Han,4 David Solecki,4 Sharon Frase,2 Antonella Bongiovanni,5 and Alessandra d’Azzo Nat Commun. 7: 11876. doi: 10.1038/ncomms11876

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Maintenance of epithelial cell polarity and epithelial barrier relies on the spatial organization of the actin cytoskeleton and proper positioning/assembly of intercellular junctions. However, how these processes are regulated is poorly understood.
Alix-mediated assembly of the actomyosin–tight junction polarity complex preserves epithelial polarity and epithelial barrier Yvan Campos,1 Xiaohui Qiu,1 Elida Gomero,1 Randall Wakefield,2 Linda Horner,2 Wojciech Brutkowski,3 Young-Goo Han,4 David Solecki,4 Sharon Frase,2 Antonella Bongiovanni,5 and Alessandra d'Azzo Nat Commun. 7: 11876. doi: 10.1038/ncomms11876

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Understanding the amazingly complex human cerebral cortex requires a map (or parcellation) of its major subdivisions, known as cortical areas. Making an accurate areal map has been a century-old objective in neuroscience.
A multi-modal parcellation of human cerebral cortex Matthew F. Glasser, Timothy S. Coalson, Emma C. Robinson, Carl D. Hacker, John Harwell, Essa Yacoub, Kamil Ugurbil, Jesper Andersson, Christian F. Beckmann, Mark Jenkinson, Stephen M. Smith & David C. Van Essen Nature (2016) doi:10.1038/nature18933

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Ascl1 regulates early development, well before neurogenesis, by repressing mesendoderm induction by VegT in Xenopus. The function of the N-terminal sequence of ASCL1 is less well understood. Further study is needed to better understand how the pre-neurula expression of Ascl1 functions as a transactivator and promotes neurogenesis. It remains unclear whether or how much Ascl1 protein is maternally stored. More studies are needed in future to unravel the function of the multifaceted cell fate regulator Ascl1.
A novel role for Ascl1 in the regulation of mesendoderm formation via HDAC-dependent antagonism of VegT Li Gao,1,* Xuechen Zhu,1,* Geng Chen,1 Xin Ma,2 Yan Zhang,1 Aftab A. Khand,1 Huijuan Shi,1 Fei Gu,1 Hao Lin,1 Yuemeng Chen,3 Haiyan Zhang,1 Lei He,1 and Qinghua Tao1 Development. 143(3): 492–503. doi: 10.1242/dev.126292

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The transforming growth factor beta (TGF?) related signaling is one of the most important signaling pathways regulating early developmental events. Smad2 and Smad3 possess differential sensitivities in relaying TGF? signaling and have distinct roles in regulating early developmental events. Future work is needed to investigate how Smad3 regulates neural lineage development in concert with canonical TGF?/Smad2 pathway at the transcriptional level.
Smad2 and Smad3 have differential sensitivity in relaying TGF? signaling and inversely regulate early lineage specification Ling Liu,1,4 Xu Liu,1 Xudong Ren,1 Yue Tian,1 Zhenyu Chen,1 Xiangjie Xu,1 Yanhua Du,3 Cizhong Jiang,3 Yujiang Fang,1 Zhongliang Liu,1 Beibei Fan,1 Quanbin Zhang,1 Guohua Jin,2 Xiao Yang,5 and Xiaoqing Zhang Sci Rep. 6: 21602. doi: 10.1038/srep21602

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We can now imagine how the genome is used during embryogenesis. The only missing piece is: what is the actual signal that tells each cell what part of the genome to sequester and to what level, and what part of the genome to leave exposed. Why is that signal confined to a particular subset of cells? Why is the signal received only at certain times during embryogenesis? We think we have found the missing signal. It is differentiation waves transmitted by the cell state splitter organelle.
The organelle of differentiation in embryos: the cell state splitter Natalie K. Gordon and Richard Gordon Theor Biol Med Model. 13: 11. doi: 10.1186/s12976-016-0037-2

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Most organisms have cells that are all totipotent, meaning each cell has the same DNA, but uses determination to select which differon to access in each cell. The main problem is then: how does determination occur, when considered as the selection of which cell uses which differon of genes?
The organelle of differentiation in embryos: the cell state splitter Natalie K. Gordon and Richard Gordon Theor Biol Med Model. 13: 11. doi: 10.1186/s12976-016-0037-2

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Differentiation waves are reasonably robust, in that they can accommodate variations in cell numbers, cell size, embryo size, and a wide range of temperature and other environmental fluctuations [...] [...] the cybernetic embryo has become a testable hypothesis. By thinking of the embryo in terms of differentiation waves that have goals in the cybernetic sense, we have a theory of how the embryo builds itself that is experimentally testable. The model only requires we accept the cell state splitter as the organelle of differentiation.
The organelle of differentiation in embryos: the cell state splitter Natalie K. Gordon and Richard Gordon Theor Biol Med Model. 13: 11. doi: 10.1186/s12976-016-0037-2

cybernetic embryo? waves that have goals? say what? :)Dionisio_{July 18, 2016
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This is real fun: watching reductionist bottom-up research of a marvelous top-down design!Dionisio_{July 18, 2016
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#1718 addendum https://www.youtube.com/embed/HXjn6srhAlYDionisio_{July 18, 2016
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That all of these interactions between genetically identical cells should somehow work themselves out in the creation of many distinct microenvironments, all in the right place at the right time, is about as plausible as having a musically untrained crowd of chattering people suddenly switch their cacophony to four part harmony and perform Mozart’s complete Ave Verum Corpus [...]
The organelle of differentiation in embryos: the cell state splitter Natalie K. Gordon and Richard Gordon Theor Biol Med Model. 13: 11. doi: 10.1186/s12976-016-0037-2

Very interesting illustration.Dionisio_{July 18, 2016
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Regulatory gene network models, like gradient models, lack any specific mechanism for defining the timing and the location of specific expression.
The organelle of differentiation in embryos: the cell state splitter Natalie K. Gordon and Richard Gordon Theor Biol Med Model. 13: 11. doi: 10.1186/s12976-016-0037-2

Duh! It was obvious from the very beginning that the required spatiotemporal complex specified information is missing. Why did it take them so long to figure out that? Oh, well! what else is new?Dionisio_{July 18, 2016
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Multicellular organisms are made of 4D spatiotemporal arrays of different cell types. There is a widespread assumption that the environment somehow determines which cells in an embryo become which kinds. Morphogens are the basis for the concept of positional information which presumes that a cell can know its position by “reading” the concentration of the molecules of the gradients and then deciding what it is supposed to do, by “looking up” its coordinates in some sort of stored table in its DNA. Morphogens are still widely taught, along with gene regulatory networks, as a full explanation of embryogenesis. There are numerous problems with the morphogen gradient model: [...] Many doubts about the functioning or existence of these so-called “morphogen” gradients have been raised, with alternatives and elaborations, and transport mechanisms other than diffusion being proposed.
The organelle of differentiation in embryos: the cell state splitter Natalie K. Gordon and Richard Gordon Theor Biol Med Model. 13: 11. doi: 10.1186/s12976-016-0037-2

Emphasis mine. The unending story continues...Dionisio_{July 17, 2016
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The cell state splitter is a membraneless organelle at the apical end of each epithelial cell in a developing embryo. Embryogenesis may be represented then as a bifurcating differentiation tree, each edge representing one cell type. In combination with the differentiation waves they propagate[how?], cell state splitters explain[how?] the spatiotemporal course of differentiation in the developing embryo.
The organelle of differentiation in embryos: the cell state splitter Natalie K. Gordon and Richard Gordon Theor Biol Med Model. 13: 11. doi: 10.1186/s12976-016-0037-2

do they really explain it or just add up more complexity to the explanation? :)Dionisio_{July 17, 2016
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Noggin4 is a Noggin family secreted protein whose molecular and physiological functions remain unknown. [...] it is important to elucidate the functions of the third sub-family of Noggins, Noggin4, which comprises members with substantially less homology with other Noggins (approximately 35%) and thus may exhibit different molecular and physiological activity. Noggin4 operates as a long-range inhibitor of a principal ligand of the canonical Wnt signalling pathway, Wnt8. It would be interesting to verify whether Noggin4, like Frzb, is also unable to antagonise Wnt3a activity. [...] it would be interesting to address a potential role for Noggin4 in blocking signalosome formation and/or function.
Noggin4 is a long-range inhibitor of Wnt8 signalling that regulates head development in Xenopus laevis Fedor M. Eroshkin,1,* Alexey M. Nesterenko,b,1,2,* Alexander V. Borodulin,1 Natalia Yu. Martynova,1 Galina V. Ermakova,1 Fatima K. Gyoeva,3 Eugeny E. Orlov,1 Alexey A. Belogurov,1 Konstantin A. Lukyanov,1 Andrey V. Bayramov,c,1 and Andrey G. Zaraisky Sci Rep. 2016; 6: 23049. doi: 10.1038/srep23049

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[...] there must be other molecules and mechanisms in the embryo that refine and shape the Nodal morphogen gradient. [...] the Nodal gradient is dependent upon diffusion, binding, and degradation of the morphogen. It will be interesting to determine how Oep/Cripto co-receptors and Lefty shape the active signaling gradient. It is not known if the ECM or HSPGs play a role in modulating the Nodal morphogen gradient [...] [...] the differential stability of Nodal ligands play key roles in shaping the Nodal gradient and activity range. [...] diffusion, extracellular interactions i.e., Nodal-receptor binding, Nodal-Lefty inhibitor binding, and selective ligand destruction collectively shape and refine the Nodal morphogen gradient.
Extracellular interactions and ligand degradation shape the nodal morphogen gradient Yin Wang,1,2,† Xi Wang,3,† Thorsten Wohland,2,3,* and Karuna Sampath eLife. 5: e13879. doi: 10.7554/eLife.13879

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The correct distribution and activity of secreted signaling proteins called morphogens is required for many developmental processes. Nodal morphogens play critical roles in embryonic axis formation in many organisms. Models proposed to generate the Nodal gradient include diffusivity, ligand processing, and a temporal activation window. But how the Nodal morphogen gradient forms in vivo remains unclear.
Extracellular interactions and ligand degradation shape the nodal morphogen gradient Yin Wang,1,2,† Xi Wang,3,† Thorsten Wohland,2,3,* and Karuna Sampath eLife. 5: e13879. doi: 10.7554/eLife.13879

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[...] HSC development in the embryo involves stage-dependent interactions between dorsal, ventral and lateral domains of the AGM region, mediated at least partly by the interplay of SCF, Shh, BMP4 and Noggin. Further detailed analysis will be required to better understand the complexity of the AGM signalling landscape in which HSC development takes place. [...] is currently unclear whether any factors become expressed in a polarized manner within the reaggregates and as such, whether polarization is also a pre-requisite for HSC maturation. How exactly HSC maturation dynamics depend on overlapping concentrations of factors requires further analysis.
Inductive interactions mediated by interplay of asymmetric signalling underlie development of adult haematopoietic stem cells Céline Souilhol,1 Christèle Gonneau,1 Javier G. Lendinez,1 Antoniana Batsivari,1 Stanislav Rybtsov,1 Heather Wilson,1 Lucia Morgado-Palacin,1 David Hills,1 Samir Taoudi,2,3,4 Jennifer Antonchuk,5 Suling Zhao,1 and Alexander Medvinskya,1 Nat Commun. 2016; 7: 10784. doi: 10.1038/ncomms10784

Dionisio_{July 14, 2016
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gpuccio
“In the end, all we can say is that the kidney knows how to regulate sodium, and we don’t!”
Yes, that seems like a very accurate statement that shows the honesty and humility of its author. Perhaps today they know much more about kidney functioning than the did back then, but new questions have appeared. Regarding my medical condition anecdote, at this point the sodium has come up within the desirable range in the last few lab results. :) But during the intensive investigation I think one doctor noted that the pituitary gland appeared sending 'unexpected' signals for the kidney to release more sodium than it should have. I'm glad to know you still look at some papers referenced here.Dionisio_{July 14, 2016
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Dionisio: Sorry for your sodium problems. Nephrology is one of those fields in medicine which are as interesting from a physiologic point of view as they are clinically frustrating. I remember that, many years ago, I was reading a nephrology textbook and, at the end of the chapter about sodium regulation, there was a statement which was more or less: "In the end, all we can say is that the kidney knows how to regulate sodium, and we don't!" I don't think that things have changed much. :)gpuccio_{July 14, 2016
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gpuccio, It's good to read your comments again! Thank you. I know of a young medical doctor -a friend of one of my children's- who after graduating from medical school and later completing the pediatric residence training, went on to complete a fellowship in pediatric nephrology. However, apparently none of them have time to read this blog. :) Last year, when I was diagnosed with hyponatremia, the doctors who treated me explored the potential endocrinology signaling association between pituitary gland, thyroid gland and electrolytes regulation in the kidneys. Maybe I did not get it exactly right, but I remember they went into something like that. I ended up being seen by various different specialists (internal medicine, nephrology, endocrinology, cardiovascular, neurology, urology). Lots of tests. MRIs did not reveal any possible tumors. Basically the exact cause wasn't identified. Lately the sodium level got back to normal, but maybe mainly through diet adjustments. :) The whole learning experience was very humbling to me (and perhaps to some of those doctors too?).Dionisio_{July 14, 2016
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[...] it is now time to thoroughly investigate the individual transport of morphogens and the intercellular communication between involved cells by actual cell biological techniques.
Special Morphological Features at the Interface of the Renal Stem/Progenitor Cell Niche Force to Reinvestigate Transport of Morphogens During Nephron Induction Will W. Minuth* and Lucia Denk Biores Open Access. 5(1): 49–60. doi: 10.1089/biores.2015.0039

it is now time to thoroughly investigate ? Why now? why not before? Wasn't "thorough investigation" the scientific approach to answer difficult questions and resolve complex problems? When did that approach change? Why? Note this is related to preceding posts @1700-1705 too.Dionisio_{July 14, 2016
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Dionisio: Thank you for this interesting link. Nephrology was indeed my first passion in medicine. The morphological and functional complexity of the kidney is absolutely amazing, and should be enough to convert any sincere neo darwinist to the cause of Intelligent (Very Intelligent) Design!gpuccio_{July 14, 2016
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Previously it was assumed that mesenchymal and epithelial cells in the renal stem/progenitor cell niche have an intimate contact and that the reciprocal transport of morphogens during induction of a nephron is based exclusively on diffusion. However, recent morphological findings illustrate that mesenchymal and epithelial cell bodies are separated by a striking interface consisting of textural extracellular matrix. Further on, projections of mesenchymal cells cross the interface to establish an intercellular communication with epithelial cells via tunneling nanotubes. Regarding the heterogeneously composed group of involved morphogens in combination with the special microenvironment in the interface and the presence of tunneling nanotubes, an exchange of morphogens alone by diffusion seems highly unlikely. Instead, due to flexibility of mesenchymal cell projections including tunneling nanotubes, it is probable that most of morphogens are transported this path at the right time, punctual site, and dosed amount. Whether microvesicles are involved in the transport of morphogens within the renal stem/progenitor cell niche has to be explored.
Special Morphological Features at the Interface of the Renal Stem/Progenitor Cell Niche Force to Reinvestigate Transport of Morphogens During Nephron Induction Will W. Minuth* and Lucia Denk Biores Open Access. 5(1): 49–60. doi: 10.1089/biores.2015.0039

Oh no! wrong assumption again? [note this commentary is not about this paper but about all previous papers that have missed the point] Why did they rush to draw a conclusion without having all the questions answered? Perhaps some questions had not been even asked yet? Why? What kind of scientific approach is that? Where did humility go? Wasn't it obvious that diffusion alone couldn't explain the spatiotemporal specificity of the morphogen distribution?Dionisio_{July 14, 2016
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Formation of a nephron depends on reciprocal signaling of different morphogens between epithelial and mesenchymal cells within the renal stem/progenitor cell niche. Previously, it has been surmised that a close proximity exists between both involved cell types and that morphogens are transported between them by diffusion. However, actual morphological data illustrate that mesenchymal and epithelial stem/progenitor cell bodies are separated by a striking interface.
Special Morphological Features at the Interface of the Renal Stem/Progenitor Cell Niche Force to Reinvestigate Transport of Morphogens During Nephron Induction Will W. Minuth* and Lucia Denk Biores Open Access. 5(1): 49–60. doi: 10.1089/biores.2015.0039

striking? Not exactly how it was assumed? Diffusion was assumed as the spatiotemporal morphogen distribution mechanism without having enough evidence to confirm it? Diffusion alone didn't answer all the associated questions?Dionisio_{July 14, 2016
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The selectivity of FGFs for different binding structures in glycosaminoglycans provides a means to probe the distribution of these binding sites in Rama 27 cell pericellular matrix and to determine the effect this has on the diffusion of the FGFs. A number of different mechanisms are likely to regulate the distribution of these binding sites [...] The high multiplicity of interactions, both between proteins and polysaccharide and between the polysaccharide-binding proteins themselves [...] is likely to produce a dynamic network of interlinked molecules. This would then be responsible for the long-range (supramolecular) structure of the pericellular matrix, which determines its spatial binding capabilities for individual proteins. [...] although extracellular matrix in cartilage is specialized, in other tissues, an analogous situation may exist, where pericellular, extracellular and basement membrane matrices may exhibit different types of supramolecular structure and consequently have different functions.
Selectivity in glycosaminoglycan binding dictates the distribution and diffusion of fibroblast growth factors in the pericellular matrix Changye Sun,1 Marco Marcello,2 Yong Li,1 David Mason,2 Raphaël Lévy,1 and David G. Fernig1 Open Biol. 6(3): 150277. doi: 10.1098/rsob.150277

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The range of biological outcomes generated by many signalling proteins in development and homeostasis is increased by their interactions with glycosaminoglycans, particularly heparan sulfate (HS). This interaction controls the localization and movement of these signalling proteins, but whether such control depends on the specificity of the interactions is not known. [...] the specificity of the interactions of proteins with glycosaminoglycans controls their binding and diffusion. Moreover, cells regulate the spatial distribution of different protein-binding sites in glycosaminoglycans independently of each other, implying that the extracellular matrix has long-range structure.
Selectivity in glycosaminoglycan binding dictates the distribution and diffusion of fibroblast growth factors in the pericellular matrix Changye Sun,1 Marco Marcello,2 Yong Li,1 David Mason,2 Raphaël Lévy,1 and David G. Fernig1 Open Biol. 6(3): 150277. doi: 10.1098/rsob.150277

What determines the specificity of the interactions of proteins? How is that specificity determined?Dionisio_{July 12, 2016
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Morphogen gradients induce sharply defined domains of gene expression in a concentration-dependent manner, yet how cells interpret these signals in the face of spatial and temporal noise remains unclear. [...] RA forms a noisy gradient during critical stages of hindbrain patterning [...] [...] cells use distinct intracellular binding proteins to attenuate noise in RA levels. Animal cells need to be able to communicate with each other so that they can work together in tissues and organs. To do so, cells release signaling molecules that can move around within a tissue and be detected by receptors on other cells. Cells responding to signals need to be able to distinguish these signals from random fluctuations (i.e., noise) [...] Morphogens are long-range signals thought to induce different cell behaviors in a concentration-dependent manner, but how such graded signals can be established in the face of noise and how they specify sharp boundaries of target gene expression remain unclear. These mechanisms are likely to be similar in other signaling systems and critical for embryonic development and adult physiology [...]
Noise modulation in retinoic acid signaling sharpens segmental boundaries of gene expression in the embryonic zebrafish hindbrain Julian Sosnik,1,2,3 Likun Zheng,2,4 Christopher V Rackauckas,2,4 Michelle Digman,1,2,5 Enrico Gratton,1,2,5 Qing Nie,1,2,4 and Thomas F Schilling eLife. 5: e14034. doi: 10.7554/eLife.14034

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