If ID is dead, why are some obsessed with shutting it down?

_{Denyse O'Leary

May 27, 2020

Academic Freedom, Culture, Darwinism, Intelligent Design}

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Do scientists think more about sex or ID? That was an Enter Laughing question at Evolution News and Science Today but it prompts reflection on why some people in science seem driven around the bend by the idea of design in nature. And others alter their message to avoid confronting the questions:

First, if the critics are right to say ID is “dead,” why devote so much time to it? Evolution News reported in 2014 that an article in the journal Nature admitted that scientists self-censor criticisms of neo-Darwinism to avoid lending credence to ID. As Laland et al. (2014) conceded: “Perhaps haunted by the spectre of intelligent design, evolutionary biologists wish to show a united front to those hostile to science.” In 2017 we observed how Laland followed his own advice, refusing to admit in a report published in Trends in Ecology and Evolution that the 2016 Royal Society meeting included strong critiques of the neo-Darwinian paradigm. Clearly, ID arguments are potent, and evolutionary biologists are aware of this — which is why they admit they don’t like to acknowledge problems in the evolutionary consensus.
Second, intelligent design’s supposed negative impact is hyped beyond reason. The notion that “financing of research” in the U.S. is being hurt by ID is laughable. ID research gets exactly zero dollars from the Federal Government. From other sources, the amount of money available to fund ID research, though not trivial, is minuscule compared to the amount of money available for evolutionary science. No evolutionary scientist has any right to complain.
Third, it’s a shame that “20 percent of their time and brain power” is going to ID because the trend in thought is now running toward government-backed censorship.
Evolution News, “Scientist Admits Biologists Are Obsessed with Intelligent Design” at Evolution News and Science Today

Ah yes. Mutterings about the need for censorship. When we don’t have a reasonable response to a troubling topic, first, we self-censor. Then we censor anyone who raises it. Sure, guys. That’ll work.

The questions are still there but only for those capable of addressing them.

Comments

I remember reading in this website a discussion where Dr Larry Moran affirmed that he knew exactly how morphogen gradients form. Does anybody remember when was that? How can one locate that discussion? Apparently the Canadian professor was right on target. Check this out: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7328709/#!po=0.427350 Interplay between morphogen-directed positional information systems and physiological signaling
how morphogen gradients are established, maintained and interpreted by cells still is not fully understood.
Dev Dyn. Author manuscript; available in PMC 2021 Mar 1. Published in final edited form as: Dev Dyn. 2020 Mar; 249(3): 328–341. Published online 2019 Dec 20. doi: 10.1002/dvdy.140 PMCID: PMC7328709 NIHMSID: NIHMS1601446 PMID: 31794137jawa_{March 2, 2021
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ID galore Bacterial Associates of a Gregarious Riparian Beetle With Explosive Defensive Chemistry Functional anatomy of the explosive defensive system of bombardier beetles (Coleoptera, Carabidae, Brachininae)OLV_{November 28, 2020
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mystery of bombardier beetles’ hot, toxic spray Biosynthetic origin of benzoquinones in the explosive discharge of the bombardier beetle Brachinus elongatulus
Bombardier beetles are well-known for their remarkable defensive mechanism. Their defensive apparatus consists of two compartments known as the reservoir and the reaction chamber. When challenged, muscles surrounding the reservoir contract sending chemical precursors into the reaction chamber where they mix with enzymes resulting in an explosive discharge of a hot noxious chemical spray containing two major quinones: 1,4-benzoquinone and 2-methyl-1,4-benzoquinone (toluquinone). Previously, it has been speculated that the biosynthesis of all benzoquinones originates from one core precursor, 1,4-hydroquinone. Careful ligation of the base of the reservoir chamber enabled us to prevent the explosive reaction and sample untransformed reservoir fluid, which showed that it accumulates significant quantities of 1,4-hydroquinone and 2-methyl-1,4-hydroquinone. We investigated the biosynthetic mechanisms leading to quinone formation by injecting or feeding Brachinus elongatulus beetles with stable-isotope-labeled precursors. Chemical analysis of defensive secretion samples obtained from 1,4-hydroquinone-d6-administered beetles demonstrated that it underwent conversion specifically to 1,4-benzoquinone. Analogously, results from m-cresol-d8 injected or fed beetles confirmed that m-cresol is metabolized to 2-methyl-1,4-hydroquinone, which is then oxidized to 2-methyl-1,4-benzoquinone in the hot spray. Our results refute the previous claim that 1,4-hydroquinone is the precursor of all substituted benzoquinones in bombardier beetles and reveal that they are biosynthetic products of two independent pathways. Most likely, the aforementioned biosynthetic channel of hydroxylation of appropriate phenolic precursors and subsequent oxidation is not restricted to bombardier beetles; it could well be a general pathway that leads to the formation of all congeners of benzoquinones, one of the most widely distributed groups of defensive compounds in arthropods.
PubMed OLV_{November 28, 2020
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Massive project reveals complexity of gene regulation
When the human genome was sequenced almost 20 years ago, many researchers were confident they'd be able to quickly home in on the genes responsible for complex diseases such as diabetes or schizophrenia. But they stalled fast, stymied in part by their ignorance of the system of switches that govern where and how genes are expressed in the body. Such gene regulation is what makes a heart cell distinct from a brain cell, for example, and distinguishes tumor from healthy tissue. Now, a massive, decadelong effort has linked the activity level of the 20,000 protein-coding human genes, as shown by levels of their RNA, to variation in millions of stretches of regulatory DNA. By looking at up to 54 kinds of tissue in hundreds of recently deceased people, the $150 million Genotype-Tissue Expression project has begun to connect the dots of how our genome works. The analysis drives home just how convoluted the interconnections between genes and their regulatory DNA can be.
OLV_{November 15, 2020
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What is a gene, post-ENCODE? History and updated definition
While sequencing of the human genome surprised us with how many protein-coding genes there are, it did not fundamentally change our perspective on what a gene is. In contrast, the complex patterns of dispersed regulation and pervasive transcription uncovered by the ENCODE project, together with non-genic conservation and the abundance of noncoding RNA genes, have challenged the notion of the gene. To illustrate this, we review the evolution of operational definitions of a gene over the past century—from the abstract elements of heredity of Mendel and Morgan to the present-day ORFs enumerated in the sequence databanks. We then summarize the current ENCODE findings and provide a computational metaphor for the complexity. Finally, we propose a tentative update to the definition of a gene: A gene is a union of genomic sequences encoding a coherent set of potentially overlapping functional products. Our definition sidesteps the complexities of regulation and transcription by removing the former altogether from the definition and arguing that final, functional gene products (rather than intermediate transcripts) should be used to group together entities associated with a single gene. It also manifests how integral the concept of biological function is in defining genes.
The classical view of a gene as a discrete element in the genome has been shaken by ENCODE
The ENCODE consortium recently completed its characterization of 1% of the human genome by various high-throughput experimental and computational techniques designed to characterize functional elements (The ENCODE Project Consortium 2007). This project represents a major milestone in the characterization of the human genome, and the current findings show a striking picture of complex molecular activity. While the landmark human genome sequencing surprised many with the small number (relative to simpler organisms) of protein-coding genes that sequence annotators could identify (?21,000, according to the latest estimate [see www.ensembl.org]), ENCODE highlighted the number and complexity of the RNA transcripts that the genome produces. In this regard, ENCODE has changed our view of “what is a gene” considerably more than the sequencing of the Haemophilus influenza and human genomes did (Fleischmann et al. 1995; Lander et al. 2001; Venter et al. 2001). The discrepancy between our previous protein-centric view of the gene and one that is revealed by the extensive transcriptional activity of the genome prompts us to reconsider now what a gene is. Here, we review how the concept of the gene has changed over the past century, summarize the current thinking based on the latest ENCODE findings, and propose a new updated gene definition that takes these findings into account.
OLV_{November 15, 2020
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Alexa ranking for comparable websites among the top 100 million active websites: <Alexa link>::<Site Link>::TSLI=<tsli>::AS={s1,s2,...}::<rank> TSLI: Total Sites Linking In AS: Associated Sites (according to Alexa) Alexa::AiG::TSLI=3,044::AS={CMI,ICR}::52,398 Alexa::CMI::TSLI=1,465::AS={AiG,ICR,BL,EN}::202,707 Alexa::EN::TSLI=833::AS={DI,TO,UD,BL}::219,613 Alexa::RTB::TSLI=788::AS={IGH}::259,957 Alexa::ICR::TSLI=1,751::AS={CMI,AiG,TO,BL}::267,172 Alexa::MM:TSLI=37::AS={}::277,264 Alexa::DI::TSLI=1,313::AS={EN}::362,614 Alexa::BL::TSLI=628::AS={CMI,EN,IGH,AiG,ICR}::365,581 Alexa::UD::TSLI=702::AS={EN,DI,TSZ}::730,919 Alexa::TO::TSLI=2,509::AS={EN,ICR,CMI}::946,327 Alexa::SW::TSLI=456::AS={UD}::1,360,878 Alexa::IGH::TSLI=54::AS={RTB,BL}::1,991,862 Alexa::PS::TSLI=41::AS={TSZ}::3,006,785 Alexa::TSZ::TSLI=58::AS={UD,PS,DI}::4,141,030 Alexa::PT::TSLI=1,127::AS={UD}::6,827,764 jawa_{October 29, 2020
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ID magnified again A flexible repertoire of transcription factor binding sites and diversity threshold determines enhancer activity in embryonic stem cells https://www.biorxiv.org/content/10.1101/2020.04.17.046664v2.full It is known that transcription factor binding sites (TFBS) are required for enhancer function, and that transcription factors, modulate enhancer activity in a cell type specific manner; however, the precise sequence code conferring enhancer activity in each cell type remains unknown. the sequence code conferring enhancer activity remains unknown. These findings reveal a TFBS diversity threshold overrides the need for optimized regulatory grammar and individual TFBS that bind specific master regulators.jawa_{October 27, 2020
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@175 Another way to look at this ranking: AiG:…….006 CMI:…….020 EN:…….030 RTB:…….030 MM:…….030 ICR:…….030 BL:…….040 DI:…….050 TO:…….090 SW:…….140 IGH:…….200 PS:…….400 TSZ:…….500 PT:…….700jawa_{October 25, 2020
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@175: links to each website. Missed UD:.......704,831 should be inserted between DI and TO.jawa_{October 25, 2020
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Alexa ranking for comparable websites among the top 100 million active websites: AiG:…….52,803 CMI:…….189,155 EN:…….222,462 RTB:…….275,900 MM:…….279,670 ICR:…….280,945 BL:…….380,056 DI:…….408,585 TO:…….815,994 SW:…….1,360,069 IGH:…….1,989,933 PS:…….3,008,511 TSZ:…….4,143,753 PT:…….6,824,100jawa_{October 24, 2020
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Websites that deal with Common Design (both for and against) Alexa ranking for comparable websites among the top 100 million active websites: AiG:…….52,803 CMI:.......189,155 EN:.......222,462 RTB:.......275,900 MM:.......279,670 ICR:.......280,945 BL:…….380,056 DI:.......408,585 TO:.......815,994 SW:.......1,360,069 IGH:.......1,989,933 PS:.......3,008,511 TSZ:.......4,143,753 PT:.......6,824,100 jawa_{October 24, 2020
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ID magnified? Cell-Cycle-Dependent ERK Signaling Dynamics Direct Fate Specification in the Mammalian Preimplantation Embryo
Despite the noisy nature of single cells, multicellular organisms robustly generate different cell types from one zygote. This process involves dynamic cross regulation between signaling and gene expression that is difficult to capture with fixed-cell approaches. To study signaling dynamics and fate specification during preimplantation development, we generated a transgenic mouse expressing the ERK kinase translocation reporter and measured ERK activity in single cells of live embryos. Our results show primarily active ERK in both the inner cell mass and trophectoderm cells due to fibroblast growth factor (FGF) signaling. Strikingly, a subset of mitotic events results in a short pulse of ERK inactivity in both daughter cells that correlates with elevated endpoint NANOG levels. Moreover, endogenous tagging of Nanog in embryonic stem cells reveals that ERK inhibition promotes enhanced stabilization of NANOG protein after mitosis. Our data show that cell cycle, signaling, and differentiation are coordinated during preimplantation development.
https://www.cell.com/developmental-cell/fulltext/S1534-5807(20)30715-2?dgcid=raven_jbs_aip_emailjawa_{October 22, 2020
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ID magnified? Vision Changes the Cellular Composition of Binocular Circuitry during the Critical Period
High acuity stereopsis emerges during an early postnatal critical period when binocular neurons in the primary visual cortex sharpen their receptive field tuning properties. We find that this sharpening is achieved by dismantling the binocular circuit present at critical period onset and building it anew. Longitudinal imaging of receptive field tuning (e.g., orientation selectivity) of thousands of neurons reveals that most binocular neurons present in layer 2/3 at critical period onset are poorly tuned and are rendered monocular. In parallel, new binocular neurons are established by conversion of well-tuned monocular neurons as they gain matched input from the other eye. These improvements in binocular tuning in layer 2/3 are not inherited from layer 4 but are driven by the experience-dependent sharpening of ipsilateral eye responses. Thus, vision builds a new and more sharply tuned binocular circuit in layer 2/3 by cellular exchange and not by refining the original circuit.
https://www.cell.com/neuron/fulltext/S0896-6273(20)30746-7?dgcid=raven_jbs_aip_emailjawa_{October 22, 2020
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More ID? Genes with spiralian-specific protein motifs are expressed in spiralian ciliary bandsjawa_{October 21, 2020
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ID magnified The Origin of Land Plants Is Rooted in Two Bursts of Genomic Novelty
Comparing 208 genomes gives insight into the role of gene novelty in plant evolution•Two bursts of genomic novelty played a major role in the evolution of land plants•Functions linked to these novelties are multicellularity and terrestrialization•The backbone of hormone signaling either predates or accompanies this transition

Understanding the diversification of plant life on Earth is still one of the major challenges in evolutionary biology.
And again? EN: Scientific Paper Reaffirms New Genes Required for Cambrian Explosionjawa_{October 21, 2020
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ID upon ID An adhesion code ensures robust pattern formation during tissue morphogenesis Convergence of paradigms yields patterns
In embryo development, spatial patterns of distinct cell types arise reproducibly. In the zebrafish spinal cord, neural progenitors form stereotypic stripe patterns despite the noisy instructive signals and large-scale cellular rearrangement required during morphogenesis. Tsai et al. show that a cell type–specific adhesion code, regulated by a Shh morphogen gradient composed of three adhesion molecules, provides adhesion specificity for three neural progenitor types and mediates patterning robustness in the zebrafish spinal cord. Although insufficient on their own, the integration of the morphogen gradient and differential adhesion mechanisms enables robust pattern formation during tissue morphogenesis.
Abstract
Animal development entails the organization of specific cell types in space and time, and spatial patterns must form in a robust manner. In the zebrafish spinal cord, neural progenitors form stereotypic patterns despite noisy morphogen signaling and large-scale cellular rearrangements during morphogenesis and growth. By directly measuring adhesion forces and preferences for three types of endogenous neural progenitors, we provide evidence for the differential adhesion model in which differences in intercellular adhesion mediate cell sorting. Cell type–specific combinatorial expression of different classes of cadherins (N-cadherin, cadherin 11, and protocadherin 19) results in homotypic preference ex vivo and patterning robustness in vivo. Furthermore, the differential adhesion code is regulated by the sonic hedgehog morphogen gradient. We propose that robust patterning during tissue morphogenesis results from interplay between adhesion-based self-organization and morphogen-directed patterning.
another code?jawa_{October 13, 2020
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ID magnified Key control mechanism allows cells to form tissues and anatomical structures in the developing embryo https://phys.org/news/2020-10-key-mechanism-cells-tissues-anatomical.html
For decades, scientists have intensively studied this process, called morphogenesis, but it remains in many ways enigmatic. different cell types express unique combinations of adhesion molecules in order to self-sort during morphogenesis. These "adhesion codes" determine which cells prefer to stay connected, and how strongly they do so, even as widespread cellular rearrangements occur in the developing embryo.
“adhesion codes” ? Another code ?jawa_{October 11, 2020
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ID galore
Regulation of stem cell fate is best understood at the level of gene and protein regulatory networks, though it is now clear that multiple cellular organelles also have critical impacts. A growing appreciation for the functional interconnectedness of organelles suggests that an orchestration of integrated biological networks functions to drive stem cell fate decisions and regulate metabolism.
https://www.frontiersin.org/articles/10.3389/fcell.2020.00591/full Let’s repeat it for the folks with poor reading comprehension: “an orchestration of integrated biological networks functions to drive stem cell fate decisions and regulate metabolism.” Better read the entire paper. No doubt that ID is the only explanationjawa_{October 11, 2020
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We're missing GPuccio's insightful technical OPs and comments.jawa_{October 10, 2020
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ID upon ID Chromatin three-dimensional interactions mediate genetic effects on gene expression RE: Regulatory Elements ChIP-seq: chromatin immunoprecipitation sequencing CRD: cis-regulatory domain TAD: topologically associated domains TRH: trans-regulatory hubs eQTL: expression quantitative trait loci
we still have a poor understanding of how noncoding genetic variations affect the regulatory machinery, which regulatory elements (REs) they perturb, and how their effects propagate along regulatory interactions.

TRHs are consistent with a higher-order chromatin organization into A and B nuclear compartments and show a signal of allelic coordination, suggesting that some of the trans associations are not transcriptionally mediated and result from a complex and higher-order 3D nucleus organization.

CRDs and TRHs essentially delimit sets of active REs involved in the expression of most genes and provide a dense genome-wide map linking REs and genes. these links vary substantially across cell types and are key factors involved in the cis and trans coexpression of genes.

Natural genetic variation outside of protein coding regions affects multiple molecular phenotypes that can differ across individuals. genomic variation affects proximal (cis) or distal (trans) gene regulation

Clustering regulatory elements and activity across individuals reveals genomic structures termed cis-regulatory domains and trans-regulatory hubs that affect gene expression. Associations between these structures and genes within and across chromosomes contribute to links between noncoding genetic variation and gene expression.

Overall, our study reveals the complexity and specificity of the cis- and trans-regulatory circuitry and its perturbation by genetic variations.
jawa_{October 10, 2020
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ID galore? A model to decipher the complexity of gene regulation
How, where and when genes are expressed determine individual phenotypes. If gene expression is controlled by many regulatory elements, what, ultimately, controls them? And how does genetic variation affect them?

Chromatin, a complex of DNA, RNA and proteins, plays important roles in protecting DNA during crucial phases of the cell cycle. Chromatin modifications therefore mediate the effects of expression factors, and eventually regulate gene expression.
A goal:
to build robust models of activation mechanisms and regulatory networks, and to understand what affects whether genes are expressed.
Discovery:
Regulatory activity appears to be organized in fully independent blocks, with series of regulatory elements on the same genomic region being all high or all low at the same time—as if regulatory elements were stuck together in genomic Lego blocks

Other geneticists had already pinpointed rather large structures—called the "topologically associating domain," or TAD—that play a role in gene regulation. However, the "blocks" here identified—named CRDs—are of much smaller size, enabling the definition of a much finer resolution map of gene expression.

the scientists found genetic variants that not only increase or decrease gene expression, but that have the power to change the very structure of these blocks by, for instance, splitting one block into two fully separated structures. By doing so, they change the landscape of regulation, and therefore gene expression.

"DNA is not a two-dimensional structure in the cell nucleus; it needs to be understood in three (or more) dimensions,"

"According to a traditional model of gene regulation, a gene enhancer must be located near the gene, on the same genomic region. Conversely, our model shows that regulatory elements could very well be on another chromosome. Because of the nuclear 3-D structure that brings regions together, a cross-talk of regions can take place in any of our 23 chromosomes, with 'trans-regulatory hubs' affecting genes anywhere."
models to decipher complexity
By incorporating the complexity of the genome into a single model, the scientists provide a tree of correlations of all regulatory elements across the whole genome.

"Every node of this tree can then be analysed to summarize the effects of that node, as well as the variability of all regulatory elements below that could be relevant to a certain phenotype,"

modeling complexity to determine how specific genetic or environmental factors contribute to somebody's risk or manifestation of a disease is exactly what "precision medicine" means.

"The more we disentangle the complexity, the easier it is to discover what we are looking for,"
jawa_{October 10, 2020
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ID on steroids?
Sequence-specific transcription factors (TFs) regulate gene expression by binding to cis-regulatory elements in promoter and enhancer DNA. While studies of TF–DNA binding have focused on TFs’ intrinsic preferences for primary nucleotide sequence motifs, recent studies have elucidated additional layers of complexity that modulate TF–DNA binding.
https://www.sciencedirect.com/science/article/abs/pii/S0959437X1730028Xjawa_{October 7, 2020
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ID galore Emergence of cooperative bistability and robustness of gene regulatory networks
Gene regulatory networks (GRNs) are complex systems in which many genes regulate mutually to adapt the cell state to environmental conditions. In addition to function, the GRNs possess several kinds of robustness. This robustness means that systems do not lose their functionality when exposed to disturbances such as mutations or noise, and is widely observed at many levels in living systems.
jawa_{October 4, 2020
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ID on steroids? Cellular Dialogues: Cell-Cell Communication through Diffusible Molecules Yields Dynamic Spatial Patterns https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6975168/
Cells form spatial patterns by coordinating their gene expressions. How a group of mesoscopic numbers (hundreds to thousands) of cells, without pre-existing morphogen gradients and spatial organization, self-organizes spatial patterns remains poorly understood.
jawa_{September 25, 2020
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What is this for: “Approval Ready Consulting - Dissertation Writing Service” ???jawa_{September 25, 2020
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@159: What did Dr Hartwell mean by “ the extent to which evolution has driven the accuracy of biological processes is really enormous. ” ??? How could that have happened? Any clues?jawa_{September 25, 2020
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Video on YouTube Dr Sue Biggins interviews Dr Leland Hartwell. Video published 2019-02-19 2020-09-16 only 2,340 views and one comment Cell Division Cycle (CDC) 2001 Nobel Prize in Physiology or Medicine Define Cell Cycle Checkpoints:
Well, we tried to define it relatively clearly, as something which is needed to arrest division when something goes wrong We certainly wondered that. And I think over the years, a lot more has been discovered.And so... you know, one of the, I think, really fundamental principles about biology, that fascinates me, is the tremendous accuracy of biological processes. So, yeast cells lose a chromosome about once in 100,000 divisions. That's remarkably precise and reproducible, especially when you watch mitosis and see the chromosomes jiggling around and everything. You wonder how they keep track of them. And I suspect that's true for all kinds of cellular processes, that normally we can't measure the accuracy because it is so accurate. And... and so the extent to which evolution has driven the accuracy of biological processes is really enormous. And it... I think it must mean that for most things that go on in biology, there's the basic machinery, there are things which repair the basic machinery when it gets in trouble, and there are things that coordinate that repair with everything else that's going on. And we probably only know the tip of the iceberg yet in terms of cell biology.
jawa_{September 16, 2020
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Here it goes again: ENCODE discovers many new transcription-factor-binding-site motifs and explores their properties https://www.nature.com/articles/nature28170jawa_{September 14, 2020
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@153, 155: “the super-enhancer concept tends to oversimplify more complex patterns of gene regulation.” Isn’t that what we see in many cases? :)jawa_{September 14, 2020
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Why don’t ID objectors post their strong counter arguments here? Simply because they lack what it takes to engage in serious scientific discussions. That’s all. Their case is doomed.jawa_{September 14, 2020
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