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	<title><![CDATA[BOL: Related items]]></title>
	<link>https://bioinformaticsonline.com/related/10659?offset=930</link>
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	<item>
	<guid isPermaLink="true">https://bioinformaticsonline.com/blog/view/44614/online-resources-on-must-read-papers-in-evolutionary-biology</guid>
	<pubDate>Fri, 26 Jul 2024 01:39:14 -0500</pubDate>
	<link>https://bioinformaticsonline.com/blog/view/44614/online-resources-on-must-read-papers-in-evolutionary-biology</link>
	<title><![CDATA[Online resources on must-read papers in evolutionary biology]]></title>
	<description><![CDATA[<pre>Online resources on must-read papers in evolutionary biology, for a literature club.<br /><br />Below is a summary of all answers that we received.

All the best,

Jana and Xiaoyan

1.       *Nick Barton:*

- The textbook "Evolution" by Nick Barton, with resources for
  exploring the literature: Barton, N. H., Briggs, D. E. G., Eisen, J.
  A., Goldstein, D. B., &amp; Patel, N. H. (2007). Evolution. Cold Spring
  Harbor Laboratory Press.

- Papers from a course named "Classics in Evolutionary Biology":

Evolutionary Synthesis
1. Haldane, J. B. S. 1932. The causes of evolution. Longmans. New York.
   (esp. Ch. IV).
2. Fisher, R. A. 1930. The genetical theory of natural selection. Oxford
   University Press, Oxford. Selected Sections - Fundamental Theorem.

Genetic Variation
1a. Lewontin, R. C., and J. L. Hubby. 1966. A molecular approach to
the study of genic heterozygosity in natural populations. II. Amount
of variation and degree of heterozygosity in natural populations of
Drosophila pseudoobscura. Genetics. 54:595-609.

1b. Sachidandam et al. 2001. A map of human genome sequence variation
containing 1.42 million single nucleotide polymorphisms. 409: 928-33.

2. Wright S., Dobzhansky T., Hovanitz W. 1942 Genetics of natural
populations VII The allelism of lethals in the third chromosome of
Drosophila pseudoobscura. Genetics 27: 363-394.

Recombination and evolution
1. Hill, W. G., and A. Robertson. 1966. The effect of linkage on limits
to artificial selection. Genet. Res. 8:269-294.

2. Maynard Smith and Haigh. 1974. The hitch-hiking effect of a favourable
gene. Genet. Res. 23: 23-35.

Understanding sequence variation
1. Begun D. J., Aquadro C. F., 1992 Levels of naturally occurring DNA
polymorphism correlate with recombination rate in Drosophila melanogaster.
Nature 356: 519-520.

2. Green R. E., Reich D., P&auml;&auml;bo S., 2010 A draft sequence of the
Neandertal genome. Science 328: 710-722.

Quantitative Genetics:  variation in complex traits
1. Galton F., 1877 Typical laws of heredity. Nature 15: 492-495-
512-514- 532-533.

2. Turelli M., 1984 Heritable genetic variation via
mutation-selection balance: Lerch's Zeta meets the abdominal
bristle. Theor. Popul. Biol. 25: 138-193.

Quantitative Genetics:  finding the genes
1. Shrimpton A. E., Robertson A., 1988 The Isolation of polygenic factors
controlling bristle score in Drosophila melanogaster II Distribution of
third chromosome bristle effects within chromosome sections. Genetics
118: 445-459.

2. Boyle E. A., Li Y. I., Pritchard J. K., 2017 An expanded view of
complex traits: from polygenic to omnigenic. Cell 169: 1177-1186.

Neutral Evolution
1. Kimura, M. 1968. Evolutionary rate at the molecular level. Science.
217:624-626.

2a. Kern A. D., Hahn M. W., 2018 The Neutral Theory in Light of Natural
Selection. Molecular Biology and Evolution 110: 21077-6.

2b. Jensen J. D., Payseur B. A., Stephan W., Aquadro C. F., Lynch M.,
Charlesworth D., Charlesworth B., 2018 The importance of the Neutral Theory
in 1968 and 50 years on: a response to Kern and Hahn 2018. Evolution 112:
2109-4.

2c. Ellegren &amp; Galtier. 2016. Determinants of genetic diversity. Nature
Reviews Genetics.

Mutation and Genetic Variability
1. Luria, S. E., and M. Delbr&uuml;ck. 1943. Mutations of Bacteria from Virus
Sensitivity to Virus Resistance. Genetics. 28(6):491-511.

2. Hill, W G. 1982. "Rates of Change in Quantitative Traits From Fixation
of New Mutations." Proceedings of the National Academy of Sciences (U.S.A.)
79: 142-45.

Testing for selection
1. McDonald &amp; Kreitman. 1991. Adaptive protein evolution at the Adh locus
in Drosophila. Nature.

2. Begun, et al. Mol. Biol. Evol. 16, 1816-1819 (1999).

3. Siddiq et al. 2016. Experimental test and refutation of a classic case
of molecular adaptation in Drosophila melanogaster.  Nature Ecology &amp;
Evolution.

The shifting balance
1. Wright, S. 1932. The roles of mutation, inbreeding, crossbreeding and
selection in evolution. Proceedings of the VI International Congress of
Genetics: 1. pp 356-366.

2. Coyne, J.A., N.H. Barton, and M. Turelli. 1997. A critique of Wright's
shifting balance theory of evolution.  Evolution 51: 643-671.

3. Barton. 2016. Sewall Wright on Evolution in Mendelian Populations and
the "Shifting Balance". Genetics.

Evolution of Sex
1.  Muller, H.J. 1964. The relation of recombination to mutational advance.
Mutation Res. 1(1):2-9

2. McDonald et al. 2016. Sex speeds adaptation by altering the dynamics of
molecular evolution. Nature.

Kin Selection, Cooperation, and Conflict
1. Hamilton, W. D. 1964. The genetical evolution of social behaviour I.
Journal of Theoretical Biology. 7:1-52.

2. Trivers, R. L. 1974 Parent-offspring conflict. American Zoologist.
14(1):249-264.

Sexual Selection
1. Zahavi, A. 1975. Mate selection - a selection of a handicap. J. Theor.
Biol. 53:205-214.

2. Kirkpatrick, M., and Ryan, M.J. 1991. The evolution of mating
preferences and the paradox of the lek. Nature. 350:33-38.

Fitness Landscapes
1. Dean, A. 1995. A Molecular Investigation of Genotype by Environment
Interactions. Genetics. 139:19-33.

2. Costanzo et al. 2010. The Genetic Landscape of a Cell. Science.

Speciation
1. Coyne, J. A., and H. A. Orr. 1989. Patterns of speciation in Drosophila.
Evolution. 43:362-381.

2. Corbett-Detig et al. 2013. Genetic incompatibilities are widespread
within species. Nature.

2.       *Marcos Antezana:*

Valen, L. v. 1975. Energy and Evolution. University of Chicago, Department
of Biology.

3.       *Remco Folkertsma:*

1. The work by Hopi Hoekstra on local adaptation and oldfield mice

2. Poelstra, J. W., Vijay, N., Bossu, C. M., Lantz, H., Ryll, B., M&uuml;ller,
I., ... &amp; Wolf, J. B. (2014). The genomic landscape underlying phenotypic
integrity in the face of gene flow in crows. Science, 344(6190), 1410-1414.

4.       *Joshka Kaufmann and Leslie Turner*

They offer us a link to 'papers every evolutionary biologist should read',
the papers are collected by Leslie Turner.
https://static1.squarespace.com/static/53e8cb7ce4b02c4bc3aeeee4/t/5ab8fcb670a6ad55c67fcdf4/1522072758665/EvoBioClassicsRefList.pdf

5.       *Sarah Stockwell*

Matt Ridley collected classic papers in evolutionary biology and printed
part of these papers in his book Evolution (see Matt Ridley. Evolution
(Univ. of Oxford Press, 2nd edition, 2004))
</pre>]]></description>
	<dc:creator>BioStar</dc:creator>
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	<guid isPermaLink="true">https://bioinformaticsonline.com/blog/view/45231/the-giant-who-walked-across-ancient-taiwan</guid>
	<pubDate>Sat, 15 Aug 2026 14:48:45 -0500</pubDate>
	<link>https://bioinformaticsonline.com/blog/view/45231/the-giant-who-walked-across-ancient-taiwan</link>
	<title><![CDATA[The Giant Who Walked Across Ancient Taiwan]]></title>
	<description><![CDATA[<p>Thousands of years ago, long before Taiwan became the island we know today, a large-bodied human walked across the landscape. We will probably never know what this individual looked like or where they travelled. But part of their story survived&mdash;in two ancient leg bones recovered from the seabed of the Penghu Channel.</p><p>The bones sat quietly in a fossil collection for years. One was part of a femur; the other, a tibia. They looked like the remains of an unusually large ancient human. But who did they belong to?</p><p>The answer came from an unexpected source: ancient proteins.</p><p>Using palaeoproteomic analysis, researchers found a molecular signature in both bones that matches the Denisovan lineage. The discovery identifies the two Penghu fossils as Denisovan and, more importantly, gives scientists their first substantial glimpse of the Denisovans' body size.</p><p>And the picture is striking.</p><p>One individual is estimated to have been about 1.8 metres tall and weighed around 83 kilograms. The other may have reached 1.9 metres and about 91 kilograms. Their leg bones rank among the largest known from Pleistocene Homo.</p><p>These were not small or fragile people.</p><p>They were powerful, heavily built humans moving through Ice Age eastern Asia.</p><p>But the bones tell an even more intriguing story. The femur has a pronounced ridge called a femoral pilaster&mdash;a feature particularly associated with modern human hunter-gatherers and increased mechanical strength during terrestrial movement. Why would a Denisovan, with an otherwise strongly archaic skeleton, possess this modern-looking feature?</p><p>Perhaps these Denisovans travelled extensively across the landscape. Perhaps their bodies were shaped by a demanding hunting lifestyle. Or perhaps, the researchers suggest, genetic exchange with early modern humans contributed to some of these features.</p><p>Their extraordinary size raises another mystery. A common expectation in human evolution is that populations living closer to the tropics tend to be smaller. Yet these Denisovans lived around 23&deg;N latitude and were exceptionally large. The researchers argue that cold climate alone cannot explain their size, pointing instead toward lifestyle and diet&mdash;including evidence that at least one Penghu individual relied heavily on meat.</p><p>So, piece by piece, the Denisovans are becoming less mysterious.</p><p>What was once a shadowy population known mainly from DNA is beginning to take physical form: large, robust, mobile humans who lived across eastern Asia and whose bodies carried a fascinating mixture of ancient and modern traits.</p><p>And perhaps the most remarkable part of this story is where it began&mdash;not in a spectacular cave discovery, but with two weathered bones lying among thousands of fossils.</p><p>The Denisovans may have left no written history. But their bones are beginning to tell one.</p><p>*Note: This research is currently a bioRxiv preprint and has not yet undergone peer review.&nbsp; Detail at&nbsp;https://www.biorxiv.org/content/10.64898/2026.08.07.743438v1.full.pdf</p>]]></description>
	<dc:creator>Jitendra Narayan</dc:creator>
</item>

<item>
  <guid isPermaLink='true'>https://bioinformaticsonline.com/researchlabs/view/45296/luo-lab-symbiosis-genomics-evolution</guid>
  <pubDate>Wed, 09 Sep 2026 03:30:30 -0500</pubDate>
  <link></link>
  <title><![CDATA[Luo Lab | Symbiosis Genomics &amp; Evolution]]></title>
  <description><![CDATA[
<p>We study the evolutionary genomics of marine invertebrates to understand their origins and diversity. Our lab combines high-throughput sequencing and single-cell transcriptomics to explore a wide range of non-model systems. We are particularly interested in how evolutionary novelty arises, with a focus on animal development and photosymbiosis.</p>

<p>Research Directions</p>

<p>Stony corals: evolution of novelty and photosymbiosis</p>

<p>Symbiotic acoels: cell type evolution and photosymbiosis</p>

<p>Animal genomes: structural evolution and gene regulation</p>

<p>https://sgel.biodiv.tw/home</p>
]]></description>
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<item>
  <guid isPermaLink='true'>https://bioinformaticsonline.com/researchlabs/view/4546/sowdhamini-lab</guid>
  <pubDate>Sun, 15 Sep 2013 09:19:12 -0500</pubDate>
  <link></link>
  <title><![CDATA[SOWDHAMINI Lab]]></title>
  <description><![CDATA[
<p>Genome sequencing projects have enormous potential for benefiting human endeavors. However, just as acquiring a language's vocabulary does not enable one to speak it, databases that list the amino acid composition of proteins do not directly tell us much about these proteins' higher-level structure and function. The most productive way to indirectly exploit these databases has been to start with the small number of proteins that are fully-characterised and to assume that other "similar" proteins will have a related structure and function. Proteins with very similar amino acid sequence are "no-brainers", but the real test, which our group largely focuses on, is to detect the "essential" similarity in proteins whose non-critical sections have experienced random rearrangements during evolution. In such cases functionally similar proteins may have less than 25% sequence overlap.</p>

<p>More @ http://www.ncbs.res.in/sowdhamini/groups_sowdhamini.htm</p>
]]></description>
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	<guid isPermaLink="true">https://bioinformaticsonline.com/news/view/12883/breaking-chromosomes-to-study-cancer</guid>
	<pubDate>Fri, 18 Jul 2014 05:42:09 -0500</pubDate>
	<link>https://bioinformaticsonline.com/news/view/12883/breaking-chromosomes-to-study-cancer</link>
	<title><![CDATA[Breaking chromosomes to study cancer !!!]]></title>
	<description><![CDATA[<p>Chromosomes are present in every cell of our body and they contain the information the body needs to develop and function properly. This information is carried in genes that are arranged along the chromosomes. There are usually 46 chromosomes in every cell. These chromosomes come in pairs, one from our mother and one from our father. The chromosomes can be sorted into 23 pairs by looking at them down a microscope.</p><p>Most people who have a balanced translocation have the right amount of chromosome material but it has been rearranged in some way. This may happen if two chromosomes swap pieces (a reciprocal translocation). In other cases two whole chromosomes may become stuck together (a Robertsonian translocation). This page describes what happens when someone has a reciprocal translocation. <br /><br />Reciprocal chromosomal translocations occur following double-strand breaks (DSBs) in DNA when a section of one chromosome is exchanged with that of another, non-homologous chromosome. These exchanges may produce a dysfunctional fusion gene that disrupts cell growth and survival pathways, such as the translocations seen in leukemia and childhood sarcomas. <br /><br />Chromosomal translocations have been well studied in cancer cell lines which are associated with two types of cancer, acute myeloid leukemia and Ewing's sarcoma, but determining how they contribute to cancer development is complicated by additional mutations and altered gene expression profiles in these cultured cells. Now, Juan Carlos Ramirez, head of the Viral Vector Facility at the Fundacion Centro Nacional de Investigaciones Cardiovasculares (CNIC) and his colleagues Raul Torres at CNIC and Sandra Rodriguez-Peralez at the Spanish National Cancer Center (CNIO) in Madrid, Spain have used a new genome editing tool, CRISPR-Cas9, to induce chromosomal translocations for the first time in a human cell line and in primary cells. The study's authors conclude by stating that the use of this technology will allow for the clarification of how and why chromosomal translocation occurs, which without doubt will allow new anti-cancer therapeutic strategies to be tackled.</p><p>Using RNA-Guided Endonuclease (RGEN) technology or CRISPR/Cas9 genome engineering technology, CNIO and CNIC researchers have shown that it is possible to obtain such chromosomal translocations. The CRISPR-Cas9 system is extremely simple to introduce a cut at the desired locus, easier to design, and cheaper than many other systems. Using the CRISPR-Cas9 system, Ramirez and his colleagues reproduced the translocations observed in Ewing&rsquo;s Sarcoma (ES) and Acute Myeloid Leukemia (AML) patient cell lines in HEK293 cells and also generated the ES translocation in human mesenchymal stem cells and the AML translocation in umbilical cord blood cells.</p><p>By focusing on chromosomal translocation without the confounding characteristics of established cell lines, these new cells lines should help answer the fundamental question of what causes a cell to become cancerous. Ramirez and his team now look forward to modeling other chromosome translocations in a variety of cell types.</p><p>Reference:</p><p>http://en.wikipedia.org/wiki/Chromosomal_translocation</p><p>http://www.nature.com/ncomms/2014/140603/ncomms4964/abs/ncomms4964.html<br /><br /></p>]]></description>
	<dc:creator>Jit</dc:creator>
</item>
<item>
	<guid isPermaLink="true">https://bioinformaticsonline.com/bookmarks/view/37794/mimicree2-genome-wide-forward-simulations-of-evolve-and-resequencing-studies</guid>
	<pubDate>Fri, 28 Sep 2018 09:21:14 -0500</pubDate>
	<link>https://bioinformaticsonline.com/bookmarks/view/37794/mimicree2-genome-wide-forward-simulations-of-evolve-and-resequencing-studies</link>
	<title><![CDATA[MimicrEE2: Genome-wide forward simulations of Evolve and Resequencing studies]]></title>
	<description><![CDATA[<p><span>MimicrEE2, a multi-threaded Java program for genome-wide forward simulations of evolving populations. MimicrEE2 enables the convenient usage of available genomic resources, supports biological particulars of model organism frequently used in E&amp;R studies and offers a wide range of different adaptive models (selective sweeps, polygenic adaptation, epistasis). MimicrEE2 runs on any computer with Java installed. It is distributed under the GPLv3 license at&nbsp;</span><a href="https://sourceforge.net/projects/mimicree2/">https://sourceforge.net/projects/mimicree2/</a><span>.</span></p><p>Address of the bookmark: <a href="https://sourceforge.net/projects/mimicree2/" rel="nofollow">https://sourceforge.net/projects/mimicree2/</a></p>]]></description>
	<dc:creator>Jit</dc:creator>
</item>
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	<guid isPermaLink="true">https://bioinformaticsonline.com/bookmarks/view/40140/alf-a-simulation-framework-for-genome-evolution</guid>
	<pubDate>Tue, 22 Oct 2019 22:05:58 -0500</pubDate>
	<link>https://bioinformaticsonline.com/bookmarks/view/40140/alf-a-simulation-framework-for-genome-evolution</link>
	<title><![CDATA[ALF--a simulation framework for genome evolution.]]></title>
	<description><![CDATA[<p style="color: #000000; font-size: small; font-style: normal; font-weight: 400; text-align: -webkit-left;"><span style="color: #4d4d4d; font-size: small; font-style: normal; font-weight: 400; text-align: left; background-color: #ffffff; float: none;">Artificial Life Framework (ALF)</span> simulates a root genome into a number of related genomes. Result files include the resulting gene sequences, true tree and true MSAs. A description of ALF can be found in the following article:</p>
<p style="color: #000000; font-size: small; font-style: normal; font-weight: 400; text-align: -webkit-left;">Daniel A Dalquen, Maria Anisimova, Gaston H Gonnet, Christophe Dessimoz: ALF - A Simulation Framework for Genome Evolution.<span>&nbsp;</span><em>Mol Biol Evol</em>, 29(4):1115-1123, April 2012.<br><a href="http://mbe.oxfordjournals.org/content/29/4/1115" target="_blank">http://mbe.oxfordjournals.org/content/29/4/1115</a></p><p>Address of the bookmark: <a href="http://alfsim.org/#index" rel="nofollow">http://alfsim.org/#index</a></p>]]></description>
	<dc:creator>Jit</dc:creator>
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<item>
  <guid isPermaLink='true'>https://bioinformaticsonline.com/opportunity/view/43769/ideaslab-workshop</guid>
  <pubDate>Wed, 02 Feb 2022 06:13:48 -0600</pubDate>
  <link></link>
  <title><![CDATA["IdeasLab"* workshop !]]></title>
  <description><![CDATA[
<p>A new, grant-funded opportunity seeks early career researchers interested<br />in life's origins: https://templetonideaslab.umbc.edu/</p>

<p>Applications are invited to an all-expenses paid position at a 5-day<br />"IdeasLab"* workshop to be held near Prague CZ in June 2022. Thirty<br />successful applicants will be drawn in equal number from the relevant<br />sectors biological evolution, A-Life anbd theoretical physics. The week's<br />activities will lead these thirty to form interdisciplinary teams which<br />each propose how they can advance frontiers of abiogenesis research. Up to<br />$5 million total funding will be available for developing these ideas<br />produced by the week's activities. Further details of the event,<br />including the online application form, are found at the link posted above</p>
]]></description>
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	<guid isPermaLink="true">https://bioinformaticsonline.com/bookmarks/view/44525/synorth-exploring-the-evolution-of-synteny-and-long-range-regulatory-interactions-in-vertebrate-genomes</guid>
	<pubDate>Mon, 06 May 2024 06:21:10 -0500</pubDate>
	<link>https://bioinformaticsonline.com/bookmarks/view/44525/synorth-exploring-the-evolution-of-synteny-and-long-range-regulatory-interactions-in-vertebrate-genomes</link>
	<title><![CDATA[Synorth: exploring the evolution of synteny and long-range regulatory interactions in vertebrate genomes]]></title>
	<description><![CDATA[<p><span>Genomic regulatory blocks are chromosomal regions spanned by long clusters of highly conserved noncoding elements devoted to long-range regulation of developmental genes, often immobilizing other, unrelated genes into long-lasting syntenic arrangements. Synorth&nbsp;</span><a href="http://synorth.genereg.net/" target="_blank">http://synorth.genereg.net/</a><span>&nbsp;is a web resource for exploring and categorizing the syntenic relationships in genomic regulatory blocks across multiple genomes, tracing their evolutionary fate after teleost whole genome duplication at the level of genomic regulatory block loci, individual genes, and their phylogenetic context.</span></p>
<p><span>More at&nbsp;https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2745767/</span></p><p>Address of the bookmark: <a href="http://synorth.genereg.net/" rel="nofollow">http://synorth.genereg.net/</a></p>]]></description>
	<dc:creator>LEGE</dc:creator>
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  <guid isPermaLink='true'>https://bioinformaticsonline.com/opportunity/view/6954/workshop-on-population-and-metagenomics-analysis-nerc</guid>
  <pubDate>Sun, 01 Dec 2013 14:25:45 -0600</pubDate>
  <link></link>
  <title><![CDATA[Workshop on population and metagenomics analysis @ NERC]]></title>
  <description><![CDATA[
<p>Workshop Overview</p>

<p>A ten-day workshop taking place between 25 February - 6 March 2014 providing detailed hands-on training for population and meta-genomics analysis for researchers with little or no background in mathematics or computing.</p>

<p>Venue: Dartington Hall, Totnes, Devon (nearest train station - Totnes)</p>

<p>Times: 25 February - 6th March 2014.</p>

<p>Arrival evening of Tuesday 25 February 2014. Departure morning of 6th March 2014. The course itself will take place 9am-12pm, 2pm-5pm and on some evenings 7pm-10pm everyday 26 February-5th March. Students are expected to attend the entire course.</p>

<p>Contact: research-events@exeter.ac.uk</p>

<p>Registration</p>

<p>The course itself is free of charged and is funded by a Professional Postgraduate Development Award from NERC.</p>

<p>A total of 30 funded places are available which cover the costs of accommodation and food, but not the cost of transportation to/from the venue.</p>

<p>An additional 10 places are available for participants from industry. The cost of accommodation and meals will need to be covered by the participants.</p>

<p>You should register your interest by 31 December 2013. Participants will be informed by 10th January 2014 as to whether they have been selected. Please note that preference will be given to researchers funded by NERC.</p>

<p>More at http://www.eventbrite.co.uk/e/nerc-workshop-on-population-and-metagenomics-analysis-tickets-8628888237</p>
]]></description>
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