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	<title><![CDATA[BOL: Related items]]></title>
	<link>https://bioinformaticsonline.com/related/10749?offset=620</link>
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	<guid isPermaLink="true">https://bioinformaticsonline.com/news/view/13226/you-and-your-friend-have-similar-dna</guid>
	<pubDate>Sun, 27 Jul 2014 20:44:05 -0500</pubDate>
	<link>https://bioinformaticsonline.com/news/view/13226/you-and-your-friend-have-similar-dna</link>
	<title><![CDATA[You and your friend have similar DNA !!!]]></title>
	<description><![CDATA[<p>New research out of Massachusetts claims that people often choose friends that are similar to them in genetics and they are more accurate than you might suppose. A study published on PNAS&nbsp;http://www.pnas.org/content/111/Supplement_3/10796.full found that people are apt to pick friends who are genetically similar to themselves - so much so that friends tend to be as alike at the genetic level as a person's fourth cousin.</p><div style="text-align: center;"><img src="http://i.kinja-img.com/gawker-media/image/upload/s--CwLwHa43--/18fbmlokxcmqcjpg.jpg" alt="image" width="300" height="271" style="border: 0px; border: 0px;"></div><p>Scientists with a long-running Framingham Heart Study looked at 1,932 people (examination of about 1.5 million markers of genetic variations), comparing unrelated friends to unrelated strangers. They found that friends shared about 1% of their genes &mdash; a percentage much higher than those shared with strangers.This new findings made it clear that people have more DNA in common with those who are selected as friends than with strangers in the same population.&nbsp;</p><p>The genes that lined up the most were olfactory genes, which deal with smell. The ones that lined up the least were immune system genes. The researchers weren't sure why that happened :/. Olfactory genes might be a straightforward explanation: People who like the same smells tend to be drawn to similar environments, where they meet others with the same tendencies.</p><p>Reference:</p><p>http://www.pnas.org/content/111/Supplement_3/10796.full</p><p>Image : http://i.kinja-img.com</p>]]></description>
	<dc:creator>Jit</dc:creator>
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	<guid isPermaLink="true">https://bioinformaticsonline.com/blog/view/44773/genetic-basis-of-tail-loss-evolution</guid>
	<pubDate>Tue, 04 Mar 2025 12:12:36 -0600</pubDate>
	<link>https://bioinformaticsonline.com/blog/view/44773/genetic-basis-of-tail-loss-evolution</link>
	<title><![CDATA[Genetic basis of tail-loss evolution]]></title>
	<description><![CDATA[<p>The paper <em>"On the genetic basis of tail-loss evolution in humans and apes (https://www.nature.com/articles/s41586-024-07095-8)"</em>, published in <em>Nature</em>, investigates the genetic mechanisms that led to the loss of tails in humans and apes. The study suggests that a specific genetic mutation, involving the insertion of an <em>Alu</em> element (a type of transposable DNA sequence), played a critical role in the evolutionary transition from tailed primates to tailless hominoids.</p><h3><strong>Key Findings of the Study:</strong></h3><ol>
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<p><strong>Alu Insertion and Tail Loss:</strong><br /> The researchers discovered an <em>Alu</em>-mediated genetic change in a common ancestor of modern apes and humans. This change disrupted the normal function of a gene involved in tail development, leading to the suppression of tail formation.</p>
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<p><strong>Gene Disruption Mechanism:</strong><br /> The <em>Alu</em> insertion was found within a regulatory region of the <em>TBXT</em> gene (also known as <em>T</em> or <em>Brachyury</em>), which is crucial for tail development in vertebrates. This insertion likely altered the gene's expression patterns, leading to tail reduction over evolutionary time.</p>
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<p><strong>Functional Evidence from Model Organisms:</strong><br /> To test their hypothesis, the researchers introduced similar genetic modifications in mice. The modified mice exhibited shortened or absent tails, supporting the idea that the identified mutation played a role in tail loss in hominoids.</p>
</li>
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<p><strong>Evolutionary Implications:</strong><br /> The findings suggest that small, random genomic changes&mdash;such as transposable element insertions&mdash;can have profound effects on body morphology. This study provides evidence that mobile DNA elements (like <em>Alu</em>) can drive major evolutionary transitions.</p>
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<p><strong>Relevance to Human Evolution:</strong><br /> Understanding the genetic basis of tail loss helps in reconstructing the evolutionary history of hominins (the lineage that includes humans and our extinct relatives). It also sheds light on how genetic variations contribute to anatomical diversity among primates.</p>
</li>
</ol><h3><strong>Significance of the Study:</strong></h3><p>This research highlights the role of transposable elements in shaping evolutionary traits and provides a concrete genetic explanation for a defining characteristic of humans and great apes. It also demonstrates how mutations in regulatory regions of developmental genes can lead to significant anatomical changes.</p>]]></description>
	<dc:creator>LEGE</dc:creator>
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  <guid isPermaLink='true'>https://bioinformaticsonline.com/researchlabs/view/856/papenfuss-lab</guid>
  <pubDate>Sun, 14 Jul 2013 12:22:28 -0500</pubDate>
  <link></link>
  <title><![CDATA[Papenfuss Lab]]></title>
  <description><![CDATA[
<p>The human genome project and similar projects in disease-causing organisms such as Plasmodium falciparum, which causes malaria in humans, have provided new tools for discovery in biology and have accelerated the development of understanding in human disease.</p>

<p>Research Area: <br />Analysis of Next Generation sequence data in cancer<br />Methods for analysis of structural variation in cancer genomes<br />Next Generation sequencing in malaria<br />Computational comparative genomics<br />Sensitive genomic sequence search techniques using hidden Markov models<br />Tasmanian devil facial tumour disease</p>

<p>Link @ http://www.wehi.edu.au/faculty_members/dr_tony_papenfuss</p>
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	<guid isPermaLink="true">https://bioinformaticsonline.com/bookmarks/view/13842/swabs-to-genomes-a-comprehensive-workflow</guid>
	<pubDate>Sun, 10 Aug 2014 03:01:21 -0500</pubDate>
	<link>https://bioinformaticsonline.com/bookmarks/view/13842/swabs-to-genomes-a-comprehensive-workflow</link>
	<title><![CDATA[Swabs to Genomes: A Comprehensive Workflow]]></title>
	<description><![CDATA[<p>The sequencing, assembly, and basic analysis of microbial genomes, once a painstaking and expensive undertaking, has become almost trivial for research labs with access to standard molecular biology and computational tools. However, there are a wide variety of options available for DNA library preparation and sequencing, and inexperience with bioinformatics can pose a significant barrier to entry for many who may be interested in microbial genomics. The objective of the present study was to design, test, troubleshoot, and publish a simple, comprehensive workflow from the collection of an environmental sample (a swab) to a published microbial genome; empowering even a lab or classroom with limited resources and bioinformatics experience to perform it.</p><p>Address of the bookmark: <a href="https://peerj.com/preprints/453.pdf" rel="nofollow">https://peerj.com/preprints/453.pdf</a></p>]]></description>
	<dc:creator>Rahul Nayak</dc:creator>
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  <guid isPermaLink='true'>https://bioinformaticsonline.com/opportunity/view/869/bioinformatics-phd-studentship-available-in-new-zealand</guid>
  <pubDate>Sun, 14 Jul 2013 13:36:30 -0500</pubDate>
  <link></link>
  <title><![CDATA[Bioinformatics PhD studentship available in New Zealand]]></title>
  <description><![CDATA[
<p>Bioinformatics PhD studentship available in New Zealand</p>

<p>The importance of transcriptional control has been explored in a burgeoning line of research over several decades; nevertheless, we are still far from having a complete picture of the regulatory mechanisms of genes and non-coding RNAs, and their influences on different phenotypes and disease states of a cell. Recent shifts towards large-scale analyses of transcriptional regulation on a sequence and epigenetic level are at the forefront of research, mainly due to sequencing technology advancements and a deeper understanding of the fundamental regulatory processes involved.</p>

<p>Arriving at a better understanding of the influence of specific parts of the overall regulatory machinery on disease states is a high priority of the group’s research agenda.</p>

<p>We are seeking an enthusiastic student to join the group as a PhD student. Applicants must have a BSc(Hons) or MSc degree in a relevant discipline and a willingness to learn and apply new techniques and work in a team. Both local and international students are encouraged to apply.</p>

<p>The studentship covers all university fees and an annual tax-exempt stipend of NZ$22,000 for three years.</p>

<p>Sebastian Schmeier recently joined Massey University and started his own research group in Auckland, New Zealand, a city regularly ranked one of the most livable in the world. This is your chance to experience the amazing Auckland lifestyle and the excitement of joining a young new science team, while staying connected to world class scientific networks.</p>

<p>To apply for the post, please send a cover letter stating your interest in the position and why you think you would be a good candidate, a Curriculum Vitae, a copy of your academic transcript, a sample of your written scientific work, and the names of three referees. Applications will be accepted until the position is filled.</p>

<p>Enquiries and applications to Sebastian Schmeier (s.schmeier@massey.ac.nz).</p>
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	<guid isPermaLink="true">https://bioinformaticsonline.com/file/view/1970/indias-own-first-drug-from-biocon</guid>
	<pubDate>Sun, 11 Aug 2013 16:05:39 -0500</pubDate>
	<link>https://bioinformaticsonline.com/file/view/1970/indias-own-first-drug-from-biocon</link>
	<title><![CDATA[India&#039;s own first drug - from Biocon.]]></title>
	<description><![CDATA[<p><span><span>Psoriasis is immune-mediated disease that effects the skin. the Disease on an average affects about 10-20 million Indians and it attacks the immune system of human beings. In generally occurs, when the immune system mistakes a normal skin cell for a pathogen, and sends out faulty signals that cause overproduction of new skin cells. <a href="http://en.wikipedia.org/wiki/Psoriasis">More at &gt;&gt;</a><br /></span></span></p><p><span><span>Biocon, India's largest publicly-held biotechnology firm, launched its second novel 'lab-to-market' molecule,<strong> Alzumab</strong>, to treat chronic plaque <strong>psoriasis</strong> at a cost 50 per cent lower than the existing one. </span></span></p><p><span><span><span><span>Biocon is bringing Alzumab (a biologic) in the form of a vial after working on it for nearly a decade. The work had initially started in a joint effort with the Center of Molecular Immunology, Havana, but Biocon took control of the programme soon after and also bought out its partner a few years ago. Biocon tell to the media that genotypic played a critical role in functional studies and clinical trial Genomics. </span></span><br /><br />The Biocon drug, at around&nbsp;₹ 7,500 a vial, will cost half as much as the currently available drugs - from Pfizer and J&amp;J - to treat psoriasis, a skin disease that causes rough red areas where the skin comes off in small pieces. A patient is usually prescribed to consume more than 40 vials in a 24-week course.<br /><br /></span></span></p>]]></description>
	<dc:creator>Jitendra Narayan</dc:creator>
	<enclosure url="https://bioinformaticsonline.com/file/download/1970" length="90484" type="image/jpeg" />
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  <guid isPermaLink='true'>https://bioinformaticsonline.com/opportunity/view/14272/lecturersenior-lecturer-level-bc-in-bioinformatics</guid>
  <pubDate>Fri, 22 Aug 2014 12:45:52 -0500</pubDate>
  <link></link>
  <title><![CDATA[Lecturer/Senior Lecturer (Level B/C) in Bioinformatics]]></title>
  <description><![CDATA[
<p>Lecturer/Senior Lecturer (Level B/C) in Synthetic Biology, Research Fellow (Level B) in Synthetic Biology &amp; Lecturer/Senior Lecturer (Level B/C) in Bioinformatics</p>

<p>Apply now Job no: 494553<br />Work type: Continuing full time<br />Vacancy type: External Vacancy, Internal Vacancy<br />Categories: Academic - Teaching and Research</p>

<p>The Faculty of Science is launching a new and innovative branch of biological science at Macquarie University – Synthetic Biology. Synthetic biology combines engineering principles with molecular biological approaches to design and construct biological devices and systems. Recent highlights in this field include the design and synthesis of a functional bacterial genome and a yeast chromosome, and generation of synthetic bacterial cells. The rational synthesis of "designer" organisms yield important insights into how organisms work and has the potential to revolutionise biotechnological applications in areas such as bioenergy and biomanufacturing.</p>

<p>Find more at http://jobs.mq.edu.au/cw/en/job/494553/lecturersenior-lecturer-level-bc-in-synthetic-biology-research-fellow-level-b-in-synthetic-biology-lecturersenior-lecturer-level-bc-in-bioinformatics</p>
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	<guid isPermaLink="true">https://bioinformaticsonline.com/videolist/watch/3963/spotlight-on-genomics-understanding-our-genes-a-step-to-personalized-medicine</guid>
	<pubDate>Mon, 26 Aug 2013 17:07:44 -0500</pubDate>
	<link>https://bioinformaticsonline.com/videolist/watch/3963/spotlight-on-genomics-understanding-our-genes-a-step-to-personalized-medicine</link>
	<title><![CDATA[Spotlight on Genomics: Understanding Our Genes - A Step to Personalized Medicine]]></title>
	<description><![CDATA[<iframe width="" height="" src="https://www.youtube-nocookie.com/embed/GQqKRkPQXmk" frameborder="0" allowfullscreen></iframe>(Visit: http://www.uctv.tv/) Learn about the essential role of genomics in the development of stem cell based therapies. Craig Venter, president and founder of the J. Craig Venter Institute and Catriona Jamieson, director for stem cell research at the UCSD Moores Cancer Center, speak about the future of personalized medicine in which genomics, the study of genes and their function, is applied to pinpoint specific treatments for patients. Sandra Dillon, a clinical trial participant, gives a patient's perspective. [7/2013] [Health and Medicine] [Show ID: 24530]]]></description>
	
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  <guid isPermaLink='true'>https://bioinformaticsonline.com/opportunity/view/14758/phd-opportunity-at-universite-de-liege-belgium</guid>
  <pubDate>Mon, 01 Sep 2014 17:16:22 -0500</pubDate>
  <link></link>
  <title><![CDATA[PhD opportunity at Université de Liège - Belgium]]></title>
  <description><![CDATA[
<p>The Bioinformatics and Systems Biology Unit of Université de Liège (Belgium) is looking for a highly motivated master student with programming skills for a PhD thesis project (4 years, fully funded) with the goal of designing computational tools that use literature, genomic and structural data in order to infer regulatory and metabolic networks.  </p>

<p>Applicants are invited to send their resume and a recommendation letter to Prof. Patrick Meyer (more details at   www.biosys.ulg.ac.be )</p>
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	<guid isPermaLink="true">https://bioinformaticsonline.com/news/view/5963/make-genomic-research-less-ethnically-biased</guid>
	<pubDate>Wed, 30 Oct 2013 16:08:17 -0500</pubDate>
	<link>https://bioinformaticsonline.com/news/view/5963/make-genomic-research-less-ethnically-biased</link>
	<title><![CDATA[Make Genomic Research Less Ethnically-Biased]]></title>
	<description><![CDATA[<p>Mexican billionaire Carlos Slim H&eacute;lu, the world&rsquo;s 2nd-richest man, is giving an additional $74 million to a genomics center in Boston in order to right a bias in the field&ndash;a kind of scientific racism, you might call it. The problem: most samples of DNA analyzed in biomedical research come from people of European descent.</p><p>Find more detail news at http://www.forbes.com/sites/erincarlyle/2013/10/30/carlos-slim-gives-another-74-million-to-make-genomic-research-less-ethnically-biased/?utm_campaign=forbesfbsf&amp;utm_source=facebook&amp;utm_medium=social</p>]]></description>
	<dc:creator>Shikha Logwani</dc:creator>
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