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

Alexa ranks in global internet engagement Web.............rank................tsli* AIG:………..46,750.............4,136 CMI:………161,817................1,884 ICR:……..207,115................2,329 EN:………..311,392................999 RTB:……...316,803.............1,018 BL:…………330,966............789 UD:………..706,183.............804 TO:………..827,407............3,013 IGH:…….1,119,605..........72 SW:…….1,379,237...........501 PS:………..1,394,344.........16 PT:……….1,502,748...........1,175 TSZ:…….[no rank].........57 tsli: total sites linking injawa_{July 5, 2020
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@123: Another way to see the relations according to Alexa stats: AIG------------BL-------------------IGH-------------------RTB |......\..................|....................................|..................................../ |..........\..............|....................................|................................../ |..............\..........|....................................|................................/ |..................\.... |.....................................|............................../ |.....................\. |.....................................|............................/ |.....................CMI..................................|........................../ |....................../..|..\.................................|......................../ |..................../....|......\.............................|....................../ |................../......|..........\..........................|.................../ |................/........|.............\.......................|................./ |............../..........|.................\...................|.............../ |............/............|....................\................|............./ |........../..............|.......................\.............|.........../ |......../................|...........................\.........|........./ |....../..................|..............................\......|....../ |.../.....................|.................................\...|.../ ICR----------TO----------------------EN ....................................................................| ...................................................PT------UD------SW .....................................................................| ...................................................................TSZ ......................................................................| ....................................................................PSjawa_{July 5, 2020
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@122: Another way to see the relations according to Alexa stats: -------AIG---BL---CMI---EN---ICR---IGH---PS---PT---RTB---SW---TO---TSZ---UD AIG:---------O------X-------------X----------------------------------------------------------- BL: ----X------------O------X-------------X--------------------------------------------------- CMI:---X-----X-------------X-----O------------------------------------------O--------------- EN:-----------X-----O---------------------------------------------------------X-------------X- ICR:----X------------X---------------------------------------------------------X--------------- IGH:----------X------------------------------------------------X------------------------------- PS:-------------------------------------------------------------------------------------X-------- PT:--------------------------------------------------------------------------------------------X- RTB:----------------------------------------X--------------------------------------------------- SW:-------------------------------------------------------------------------------------------X- TO:-------------------X------X------X---------------------------------------------------------- TSZ:------------------------------------------------X-----------------------------------------X- UD:--------------------------X----------------------------O------------O------------X-------- -------AIG---BL---CMI---EN---ICR---IGH---PS---PT---RTB---SW---TO---TSZ---UDjawa_{July 4, 2020
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Alexa ranks in global internet engagement AIG:...........47,242......CMI, ICR CMI:.........151,923.......AIG, BL, EN ICR:........200,369.......CMI, AIG, TO EN:...........302,714.......TO, UD, BL BL:............319,667.......EN, IGH, AIG RTB:.......335,069......IGH UD:...........745,610.......EN, TSZ TO:...........763,600.......EN, ICR, CMI IGH:.......1,223,524.......RTB, BL SW:.......1,379,954.......UD PS:...........1,395,116.......TSZ PT:..........1,431,438.......UD TSZ:.......[no rank].......UD, PS PS has shown a tremendous increase in internet traffic lately. TSZ has done so poorly that it's off the Alexa radar. AIG: Answers in Genesis BL: Biologos CMI: Creation Ministries International EN: Evolution News ICR: Institute for Creation Research IGH: Is Genesis History? PS: Peaceful Science PT: Panda's Thumb RTB: Reasons to Believe SW: Sandwalk (Dr Larry Moran) TO: Talk Origins TSZ: The Skeptical Zone UD: Uncommon Descentjawa_{June 29, 2020
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ID is the only empirically reasonable explanation for this: Neurogenesis and Specification of Retinal Ganglion Cells
Across all species, retinal ganglion cells (RGCs) are the first retinal neurons generated during development, followed by the other retinal cell types. How are retinal progenitor cells (RPCs) able to produce these cell types in a specific and timely order?

the ciliary marginal zone is a new stem cell niche in mice contributing to retinal neurogenesis, especially to the generation of ipsilateral RGCs.

RGCs are composed of many different subtypes that are anatomically, physiologically, functionally, and molecularly defined.

Retinal ganglion cells (RGCs) are the sole output neurons from the retina and thus integrate and transmit all visual information to the brain. How are these RGCs generated during development?

Over recent decades, much progress has been made to improve the understanding of RGC neurogenesis and differentiation. The current view is that retinal progenitor cells in vertebrates can generate different retinal types in a stochastic manner but with a probabilistic bias for some cell types that change during development. This model could explain why all retinal cell types can be generated at any given developmental time but with a different probability, ending up with RGCs generated mostly early on and rod photoreceptors later.

The extrinsic and intrinsic factors that regulate the cell fate determination are being isolated, with compelling evolutionary conserved factors initially identified in the more deterministic neurogenesis of the drosophila eye.

However, two aspects remain to be established: (1) how the developmental expression of these factors is regulated, and (2) how the change in cell fate probabilities occur over time.

The transcription factors that regulate RGC neurogenesis are identified: Atoh7 and Pou4f2 appear as the key regulators with several transcription factors in between. As RGCs are not a homogeneous population, several studies have tried to identify the molecular determinants and/or markers of RGC subtypes. This characterization was done initially by combinatorial expression of various transcription factors or markers for different types of RGCs. However, the recent emergence of single-cell RNA sequencing technology will hopefully allow the identification of new markers for RGC subtypes but also to determine their specification pathways during development. In the future, studies will undoubtedly link molecular specification of RGC subtypes with their brain connectivity to decipher the molecular mechanisms that are at hand. Finally, understanding the developmental mechanisms determining the specification of retinal cells is crucial for the efficient, targeted generation of retinal cells from induced pluripotent stem cells of patients for research on the human retinal neurogenesis and also potential therapeutic strategies.
OLV_{June 28, 2020
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More ID evidences OTX2 represses sister cell fate choices in the developing retina to promote photoreceptor specification
During vertebrate retinal development, subsets of progenitor cells generate progeny in a non-stochastic manner, suggesting that these decisions are tightly regulated. However, the gene-regulatory network components that are functionally important in these progenitor cells are largely unknown.

OTX2 is required for the generation of photoreceptors, but also for repression of specific retinal fates and alternative gene regulatory networks. These include specific subtypes of retinal ganglion and horizontal cells, suggesting that in this context, OTX2 functions to repress sister cell fate choices.

Taken together, the current study proposes a model in which OTX2 serves as a key positive regulator of photoreceptor genesis from restricted RPCs, while repressing specific subtypes of other retinal fates (Figure 7M). At the gene regulatory network level, OTX2 represses key transcription factors involved in non-photoreceptor cell types (Figure 7N). Further combined use of the single cell sequencing/CRISPR gene editing approach with variation of time, targeted genes, and labeled cell populations will provide a powerful genetic strategy to examine developmental gene regulatory networks.
OLV_{June 23, 2020
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More support for ID Mapping the cis-regulatory architecture of the human retina reveals noncoding genetic variation in disease
Regulation of gene expression is critical for all complex biological processes including vision. Mutations within cis-regulatory elements (CREs) can disrupt gene expression and contribute to human diseases. However, it is challenging to screen for mutations within CREs that affect vision because the genomic locations and mechanisms of action of these elements are largely unknown. Here, we take advantage of advances in epigenomic and transcriptomic profiling techniques to identify and characterize CREs in three regions of the human eye commonly affected in visual disorders. Our data identify shared and unique CREs in each region, reveal the combinatorial binding of TFs, and provide a resource for understanding the role of noncoding genetic variation in visual disorders.

The interplay of transcription factors and cis-regulatory elements (CREs) orchestrates the dynamic and diverse genetic programs that assemble the human central nervous system (CNS) during development and maintain its function throughout life. Genetic variation within CREs plays a central role in phenotypic variation in complex traits including the risk of developing disease. We took advantage of the retina, a well-characterized region of the CNS known to be affected by pathogenic variants in CREs, to establish a roadmap for characterizing regulatory variation in the human CNS. This comprehensive analysis of tissue-specific regulatory elements, transcription factor binding, and gene expression programs in three regions of the human visual system (retina, macula, and retinal pigment epithelium/choroid) reveals features of regulatory element evolution that shape tissue-specific gene expression programs and defines regulatory elements with the potential to contribute to Mendelian and complex disorders of human vision.
OLV_{June 23, 2020
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More evidences favoring ID Enhancer transcription identifies cis-regulatory elements for photoreceptor cell types
Identification of cell type-specific cis-regulatory elements (CREs) is crucial for understanding development and disease, although identification of functional regulatory elements remains challenging. We hypothesized that context-specific CREs could be identified by context-specific non-coding RNA (ncRNA) profiling, based on the observation that active CREs produce ncRNAs. We applied ncRNA profiling to identify rod and cone photoreceptor CREs from wild-type and mutant mouse retinas, defined by presence or absence, respectively, of the rod-specific transcription factor (TF) Nrl. Nrl-dependent ncRNA expression strongly correlated with epigenetic profiles of rod and cone photoreceptors, identified thousands of candidate rod- and cone-specific CREs, and identified motifs for rod- and cone-specific TFs. Colocalization of NRL and the retinal TF CRX correlated with rod-specific ncRNA expression, whereas CRX alone favored cone-specific ncRNA expression, providing quantitative evidence that heterotypic TF interactions distinguish cell type-specific CRE activity. We validated the activity of novel Nrl-dependent ncRNA-defined CREs in developing cones. This work supports differential ncRNA profiling as a platform for the identification of cell type-specific CREs and the discovery of molecular mechanisms underlying TF-dependent CRE activity.
OLV_{June 23, 2020
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Game over! ID wins by KO! Studying DNA Double-Strand Break Repair: An Ever-Growing Toolbox
To ward off against the catastrophic consequences of persistent DNA double-strand breaks (DSBs), eukaryotic cells have developed a set of complex signaling networks that detect these DNA lesions, orchestrate cell cycle checkpoints and ultimately lead to their repair. Collectively, these signaling networks comprise the DNA damage response (DDR).

Our capacity to create DSBs in a programed manner and in such a way that is compatible with a set of diverse methodologies to investigate the events that follow DNA damage, has led to our current deep understanding of the DDR. The induction of DSBs at random locations using different sources of radiation or genotoxic compounds, provides the easiest approach to analyze the recruitment kinetics of proteins to sites of DNA damage and is a powerful strategy to temporally resolve the sequence of DNA repair events. The development of methods to induce annotated DNA breaks at transgenic loci inserted in the genome, or at endogenous loci (restriction enzymes, CRISPR/Cas9) allowed the analysis of the DDR at molecular resolution and were instrumental in disclosing functional links between the DDR and processes such as transcriptional, chromatin dynamics, and DNA replication. Yet all the tools described here display significant drawbacks. For instance, nucleases-induced DSBs undergo consecutive cycles of repair/cleavage until these have been mutated, calling for caution when investigating DNA repair using these tools. A major challenge is now to refine these DSB-inducible systems and the subsequent methodologies to analyze repair in order to overcome these limitations.
OLV_{June 23, 2020
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AiG:.......47,223....... EN:.......296,884....... TO:.......769,013....... UD:.......805,441....... SW:.......1,367,722....... PT:.......1,419,233....... PS:.......2,651,165....... What happened to TSZ? Fell off the Alexa radar?jawa_{June 22, 2020
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@44: Dr Swamidass would require that ID doesn’t limit to pointing to design but rather explains how the design was done. I respect his opinion, but that’s just his opinion. When I open the hood of a 2020 RAV4 XLE AWD Hybrid and someone explains to me very roughly how that engine works, I must conclude that what I’m looking at must have been designed. However, I still don’t have to know much, or anything at all, about how the design was done or the identity of the designer. Actually, given the average Joe’s poor knowledge of mechanical engineering, chemical engineering and electrical engineering, which are disciplines I assume associated with designing such a car, a rough technical explanation of how the design was done could easily blow Joe’s mind. In the case of biology, the problem increases in complexity by orders of magnitude. If we see how some complex object functions, we may imply design even without understanding who designed it or how it was designed.jawa_{June 20, 2020
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There are many direct or indirect ID evidences in this paper: Strategies and prospects of effective neural circuits reconstruction after spinal cord injury
Spinal cord injury (SCI) is a severely disabling disease that leads to loss of sensation, motor, and autonomic function

Due to the disconnection of surviving neural elements after spinal cord injury (SCI), such patients had to suffer irreversible loss of motor or sensory function, and thereafter enormous economic and emotional burdens were brought to society and family.

The pathophysiology of SCI is complex and multifaceted, and its mechanisms and processes are incompletely understood.

In this review, we summarize the recent progress in biological and engineering strategies for reconstructing neural circuits and promoting functional recovery after SCI, and emphasize current challenges and future directions.

It is believed that in the future we can analyze and record the nerve signals, and regulate the nerve signals through cell transplantation and molecular regulation after SCI. By stimulating local nerve circuits related to sensorimotor control and spinal cord autonomy, the protection, maintenance and even re-bridging of nerve circuits can be achieved. The relevant nerve circuits are fine-tuned, and then the corresponding nerve circuits are trained and strengthened by various rehabilitation methods. It can help the individual with SCI to resume autonomous movement as soon as possible, and ultimately promote the research and treatment of SCI to achieve more enormous breakthroughs in many fields.
OLV_{June 18, 2020
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Evidences that support ID keep coming out of research: Discovery of genes required for body axis and limb formation by global identification of retinoic acid–regulated epigenetic marks
Identification of target genes that mediate required functions downstream of transcription factors is hampered by the large number of genes whose expression changes when the factor is removed from a specific tissue and the numerous binding sites for the factor in the genome. Retinoic acid (RA) regulates transcription via RA receptors bound to RA response elements (RAREs) of which there are thousands in vertebrate genomes. Here, we combined chromatin immunoprecipitation sequencing (ChIP-seq) for epigenetic marks and RNA-seq on trunk tissue from wild-type and Aldh1a2-/- embryos lacking RA synthesis that exhibit body axis and forelimb defects. We identified a relatively small number of genes with altered expression when RA is missing that also have nearby RA-regulated deposition of histone H3 K27 acetylation (H3K27ac) (gene activation mark) or histone H3 K27 trimethylation (H3K27me3) (gene repression mark) associated with conserved RAREs, suggesting these genes function downstream of RA. RA-regulated epigenetic marks were identified near RA target genes already known to be required for body axis and limb formation, thus validating our approach; plus, many other candidate RA target genes were found. Nuclear receptor 2f1 (Nr2f1) and nuclear receptor 2f2 (Nr2f2) in addition to Meis homeobox 1 (Meis1) and Meis homeobox 2 (Meis2) gene family members were identified by our approach, and double knockouts of each family demonstrated previously unknown requirements for body axis and/or limb formation. A similar epigenetic approach can be used to determine the target genes for any transcriptional regulator for which a knockout is available.

In addition to H3K27ac and H3K27me3 epigenetic marks that are quite commonly observed near genes during activation or repression, respectively, it is likely that further ChIP-seq studies that identify RA-regulated binding sites for coactivators and corepressors will provide additional insight into RA target genes and transcriptional pathways. Such knowledge is essential for determining the mechanisms through which RA controls developmental pathways and should be useful to address RA function in adult organs. A similar epigenetic approach can be used to determine the target genes for any transcriptional regulator for which a knockout is available, thus accelerating the ability to understand gene regulatory networks in general.
OLV_{June 18, 2020
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BobRyan @111: Very well stated. Again. Thanks!jawa_{June 17, 2020
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Jawa: If truth and fact are removed, you can replace it with anything you wish. Socialists do not value either, since neither supports their belief in the idea of Marx over the reality of what has been tried. Men and women are biologically different. Men have more gray matter, women have more white matter. Testosterone produce more calcium then estrogen, which leads to stronger and denser bones in men. Men have a lung capacity 50% greater than women. There is a Rabbinical saying that goes along the lines of the following, God did not choose to take a bone from Adam's foot, since he did not want man to trample on a woman. God did not choose to take a bone from Adam's head, since he did not want woman to lead man. God chose the rib from Adam so man and woman can stand side by side. Men and women balance each other out. A boy who is taught there is no difference between boys and girls does not learn the important lesson of not hitting girls. They are not told that women are physically weaker than men due to biology and men should respect women. We are seeing an increase in domestic abuse by these same boys who grew up in a world without differentiation between the two sexes.BobRyan_{June 17, 2020
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Did somebody notice the trend in biology research discoveries lately? It seems increasingly to be in the area of controls. Is this a correct perception? If this is the case, what does it mean for whatever is left of the Darwinian micro-2-macro extrapolation?jawa_{June 17, 2020
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We’ve had professors Art Hunt (u Kentucky) and Larry Moran (u Toronto) engaged in discussions here in UD, but for some reason they quit when the discussion gets too technical. What kind of science professors are they? How can they still rule academics while being so scientifically weak? Does anybody understand it?jawa_{June 17, 2020
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BobRyan @107: Wow! That’s a really interesting association I didn’t realize. Thanks!jawa_{June 17, 2020
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Jawa: You're welcome. Darwinists throw out logic and reason, which is the reason for the birth of the whole WOKE nonsense.BobRyan_{June 17, 2020
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BobRyan @104: I agree. Very interesting point. Thanks! We’ve had professors Art Hunt (u Kentucky) and Larry Moran (u Toronto) engaged in discussions here in UD, but for some reason they quit when the discussion gets too technical. What kind of science professors are they?jawa_{June 17, 2020
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@102:
RING E3 ligases switch between active and inactive states through precise regulatory control that ensures the specificity and timing of polyubiquitination events. Activators, inhibitors and posttranslational modifications of RING E3s coordinate to control accurate cell cycle timing.
precise regulatory control? ensures the specificity and timing? coordinate to control accurate cell cycle timing? How?jawa_{June 17, 2020
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Jawa @ 103 Don't you know challenging their beliefs are verboten. There is nothing scientific about Darwinists worldview. Cult members never like to be called out for being part of a cult. They believe the universe magically came into existence, since the universe created itself out of nothing. They believe life originated by magic. They believe macro-evolution to be fact, when there are no facts in science. Since science is based on what is observable at any given time, future generations may observer something that contradicts existing hypothesis and theories. They cannot even bring themselves to admit this simple truth regarding science.BobRyan_{June 17, 2020
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I’ve been criticized for taking advantage of the scientific weaknesses of the ID objectors because it’s well known they lack valid arguments to engage in a serious discussion here. Sorry for making that impression, but I’m just offering a friendly invitation to present objections. They could invite the distinguished scientists Dr Art Hunt and Dr Larry Moran to come back and present their counter arguments. They know they’re always welcome here. It’s not my fault that they can’t stand the heat and run for the hills. :)jawa_{June 17, 2020
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@101: ID unopposedly unleashed
The conjugation of Ub onto proteins is a key cellular process that mediates eukaryotic protein regulation. Polyubiquitination of targeted substrates (the linkage of several ubiquitins onto a single target) can induce changes to subcellular localization, alter protein function or lead to proteasomal degradation, an important aspect of cell cycle control. As severe consequences result from the dysregulation of polyubiquitination, namely several cancers and developmental dis-orders, this process must be tightly controlled.
tightly controlled? Hmm...jawa_{June 17, 2020
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ID unleashed Ubiquitin chain-elongating enzyme UBE2S activates the RING E3 ligase APC/C for substrate priming https://www.nature.com/articles/s41594-020-0424-6
The interplay between E2 and E3 enzymes regulates the polyubiquitination of substrates in eukaryotes. Among the several RING-domain E3 ligases in humans, many utilize two distinct E2s for polyubiquitination. However, the potential coordination between these steps in ubiquitin chain formation remains undefined. Our work reveals an unexpected model for the mechanisms of RING E3–dependent ubiquitination and for the diverse and complex interrelationship between components of the ubiquitination cascade.
“unexpected model for the mechanisms”? There they go again. What else did they expect?jawa_{June 17, 2020
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@99: PDF full text of paywall paper: https://www.researchgate.net/prwaklofile/Mingyuan_Zhu4/publication/341628298_Robust_organ_size_requires_robust_timing_of_initiation_orchestrated_by_focused_auxin_and_cytokinin_signalling/links/5edeab5e45851516e661912b/Robust-organ-size-requires-robust-timing-of-initiation-orchestrated-by-focused-auxin-and-cytokinin-signalling.pdfjawa_{June 16, 2020
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ID unleashed “Robust organ size requires robust timing of initiation orchestrated by focused auxin and cytokinin signalling” https://www.nature.com/articles/s41477-020-0666-7jawa_{June 15, 2020
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ID unleashed “what sets the tempo and manages the order of developmental events? Are the order and tempo different between species? How is the sequence of multiple events coordinated?“ https://dev.biologists.org/content/145/12/dev164368jawa_{June 15, 2020
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ID unleashed Subcellular Spatial Transcriptomes: Emerging Frontier for Understanding Gene Regulation http://symposium.cshlp.org/content/early/2020/06/01/sqb.2019.84.040352.longjawa_{June 14, 2020
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ID unleashed Deciphering eukaryotic gene-regulatory logic with 100 million random promoters https://www.nature.com/articles/s41587-019-0315-8 How transcription factors (TFs) interpret cis-regulatory DNA sequence to control gene expression remains unclear, largely because past studies using native and engineered sequences had insufficient scale. TF activity depends on binding-site strand, position, DNA helical face and chromatin context.jawa_{June 14, 2020
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