When we announced the earlier module (Scripting for Biology – Online Virtual Classroom-based Module), we received a number of requests from Asian countries and sadly could not include them due to the differences with US time zone. This time, we are starting a new module to be held in Asian daytime so that students from Asia can participate.
The objective of this module is to introduce those, who never did programming, to scripting languages like python, PERL and GO. Classes will start from Oct 23 and take place every Friday at 1 PM Chinese time and or 10:30 AM Indian time. Please email [email protected], if you like to join.
The classes are chat-based and, in parallel, students write their code by logging into cloud accounts provided by us. We monitor the code they are writing and help each of them individually (through private message), if they are stuck. The examples we choose are related to solving biological problems, but they also illustrate various computer science issues (algorithm,, data structure, scaling) at an introductory level. For the current module, we initially allocated 1 hour 15 minutes per class, but the discussions tend to continue for 1.5-2 hours. Therefore, in the new module, we are allocating at least 2 hours for each session.
Using our current experience, we are making changes to the format in how the topics are being taught. In the new format, the topic will be split into eight levels, and students, who are comfortable with one level, can proceed to the next one. That way, if someone misses a class or finds the topic for a day difficult, that student can repeat the same level instead of being forced to proceed to the next level. Everyday there will be eight chat-based classrooms open for eight levels, and each student will join one of those rooms on a day.
We are working on posting all course-related materials online so that the topics being taught at each level become clear. Moreover, students will have access to their chat transcript and cloud account outside class hours so that they can practice in their own time from the posted materials. Based on feedback we received from the current module, students are finding the chat transcripts very useful.
Well, we do not know whether he really is, but anybody would be in his position. Competition has been showing up from everywhere, including short-read sequencing machine of BGI and long-read sequencers of Oxford nanopore and Pacbio. Among those, the last one’s developments are funded by Roche, whose offer to buy Illumina was rejected by him a few years back. Will the Swiss company have the last laugh?
Illumina’s stock crashed by almost half within a short span of three months, and is at 52 week low. Negative stories are showing up increasingly at financial sites – “Illumina Sales Disappoint, Will Continue to Do So“. Stock of a company is like its currency. Imagine your country’s currency crashing by 50% in 3 months !
Things were quite opposite a few months back, when one had to search hard to find anything negative about the company. All geniuses everywhere predicted sunny skies, be it Matthew Harper, Luke Timmerman or MIT Tech Review.
“a strategic inflection point is a time in the life of business when its fundamentals are about to change. that change can mean an opportunity to rise to new heights. But it may just as likely signal the beginning of the end”
“The strategic inflection point is the time to wake up an listen”
“People in the trenches are usually in touch with impending changes early”
“The person who is the star of previous era is often the last one to adapt to change, the last one to yield to logic of a strategic inflection point and tends to fall harder than most.”
“Business success contains the seeds of its own destruction. The more Successful you are, the more people want a chunk of your business and then another chunk and then another until there is nothing”
“The Lesson is, we all need to expose ourselves to the winds of change”
“While the story is unique to Intel, the lessons, I believe, are universal”
“If existing management want to keep their jobs when the basics of the business are undergoing profound change, they must adopt an outsider’s intellectual objectivity. They must do what they need to do to get through the strategic inflection point unfettered by any emotional attachment to the past. That’s what Gordon and I had to do when we figuratively went out the door, stomped out our cigarettes and returned to do the job.”
Others may argue about similarities with previous large drop in the Illumina stock during 2007-2009. After that period, company came out even stronger.
Manolis Kellis, professor of computer science at MIT, addressed the Bio-IT World Conference on efforts to revolutionize the study of human disease by bridging the gap between genetics and epigenetics.
Kellis uses genomic datasets to discover relationships between single nucleotide polymorphisms (SNPs) and epigenetic regulation. Previously, these data sets of genomic variation were used to derive associations between SNPs and specific diseases in so-called genome-wide association studies (GWAS). Kellis’s research goes one step further. “We wanted to find out what the molecular mechanism is for this association,” he said.
Over the past five years, there has been an explosion of research on the statistical associations between specific SNPs and the likelihood an individual would get a disease. This paradigm led researchers to look for specific genes that caused a disease phenotype. The list of contributing genes for complex diseases, such as Crohn’s disease or type 2 diabetes, can run into the dozens, yet only explain a fraction of the heritability of the diseases.
What Kellis’s research shows, though, is that diseases are actually caused by subtle contributions from a huge number of regulatory variants. “If we rank all the SNPs based on the association with a disease,” Kellis said, “we find that there are not 10 or 20, but thousands of regions that weakly contribute to the disease.”
Results from that research were published in early 2015.
WHEN SCIENTISTS SEQUENCED the human genome a decade ago, they hoped to unlock the code of life, the sequence of molecules lined up in every cell that, summed together, made a person a person—and possibly reveal new ways to understand and treat diseases. But the results turned out to be opaque. Biologist Eric Lander, who helped lead the effort, famously summed up the results in seven words: “Genome: Bought the book; hard to read.”
So the research community went looking for CliffsNotes. A decade ago scientists started looking into the “epigenome,” chemical modifications to DNA that tell cells which genes to turn on or turn off. This week that project got a huge data dump—24 journal articles laying out what the genomicists know so far about 111 different cell types, the inner lives of brains, hearts, blood, and skin. “It is giving us a view of the living, breathing genome in motion, as opposed to a static picture of DNA,” says Manolis Kellis, a computational biologist at MIT who worked on three1 of the new papers.
Just about every cell in a human body has the same DNA, packaged into the same chromosomes. But cells differentiate, growing into different tissue types with different functions. The epigenome works through molecules like methyl and acetyl groups that wheedle their way into DNA, exposing different genes to the machinery that reads them and makes proteins. That helps control when or whether those proteins get made at all, and it’s also critical to that process of differentiation. “In each cell type, it unravels just the right genes,” says Brad Bernstein, a biologist at Harvard University. “It unravels just the right switches.
Since then, the world had seen a boom of ‘convinving’ epigenetics studies explaining all kinds of human troubles. A few examples are given below.
Trauma Has Genetic Impact for Native Americans
Native American communities across the United States are struggling with poverty, alcoholism, high rates of diabetes, PTSD and depression. Historically, these issues have been attributed to systemic problems like racism that makes it challenging to leave the reservation, but recent research suggests the issues facing the Native American community run deeper than that. So much deeper, in fact, that they’re found within their genes, thanks to a fascinating pattern of genetic evolution and inheritance known as epigenetics.
The Holocaust is still traumatizing the children of survivors on a genetic level
World War II saw countless crimes against Jews. Millions were killed, and those who survived had their lives permanently scarred. But the harm may not have stopped there. A new study has found that the trauma experienced by Holocaust survivors caused genetic changes, which can be passed down to their children.
Epigenetic ‘tags’ linked to homosexuality in men
The biology of sexual orientation has been one of the most vexing — and politically charged — questions in human genetics. For the first time, researchers have found associations between homosexuality and markers attached to DNA that can be influenced by environmental factors.
Twin studies and family trees provide strong evidence that sexual orientation is at least partly genetic. When one identical twin is gay, there is about a 20% chance that the other will be as well1. But because this rate is not 100%, it is thought that environmental factors play a role as well. One of the best characterized is the ‘older brother effect': the chance of a man being gay increases by 33% for each older brother he has2. The reason is not clear, although one hypothesis holds that the mother’s immune system begins to react against male antigens and alter the fetus’s development.
Doctors using epigenetics to treat migraines
One in four people suffer from migraine headaches and often they’re sent to their optometrist to see if the cause is vision related.
At Dr. Scott Sedlacek’s eye center in Olmsted Falls, OH he’s using epigenetics to get to the root cause of the headache.
XR Epigenetic testing is a cheek swap and a small blood sample.
It tells you what foods are right for your body chemistry but also what you’re missing.
Dr. Sedlacek has been offering this testing for the past three years.
“Most people are eating foods that are not thought to be bad, but they’re bad for them because we’re all so unique and individual,” Sedlacek said.
Dr. George Rozakis is a bioengineer and ophthalmologist.
“We have an astonishing rate of 97 percent success. We did a study in 34 patients. Thirty-three of the 34 had a profound improvement. They were all very difficult to treat migraine patients,” Rozakis said.
Rozakis says epigenetics is not new. It’s been studied for various health conditions, including ADHD, Autism and Lupus.
After sanctioning poor countries around the world, the USA/EU-stanians got taste of their own medicine in a small way, and they do not like it at all. Some of you forwarded us this link from Science magazine about Treefinder. After doing minimal due diligence, it seemed obvious to us that the Science story was full of lies, and Gangolf Jobb was protesting against the endless warfare of USA, also supported by many EU governments. Also, based on the same Science news, Sandra Baldauf came across as a greedy, exploitative lady. The tenure system was originally created to make sure the academics could complain against the injustices conducted by their funders without getting fired, but now the academic parasites get money from various government agencies and never bother to complain against government policies (such as – Doctors Without Borders airstrike: US alters story for fourth time in four days). Why should the public pay for permanent jobs and pensions of people like Sandra Baldauf?
Anyway, those are our own opinions. To hear the views of Gangolf Jobb and Sandra Baldauf, we emailed both of them asking for interviews or comments. We are happy to share with you the replies of Gangolf Jobb, the author of Treefinder, about his decision to make recent license change. We believe his form of peaceful protest should be praised and not criticized. Baldauf did not bother to respond.
I came across your website after reading about the recent license change notice of treefinder. Thanks for agreeing about the interview in our blog.
1. Please tell us a bit about the unique features of treefinder and why researchers like to use it.
Gangolf: Treefinder is fast and convenient, and is using maximum-likelihood. It does not only compute a tree quickly, but also displays it when finished, together with the measures of support. It also provides some other analyses, which are useful in the context, such as the estimation of divergece times, also with measures of support. It also allows hypothesis testing and model selection. Without Treefinder, one would have to use several different programs from different authors, which are not always compatible, neither with their data formats nor with their models and methods used, and each comes with a different user interface one must first get used to. Treefinder saves the researcher time and nerves.
2. In Feb, you wrote – “Starting from 1st February 2015, I do no longer permit the usage of my TREEFINDER software in the USA”, and now you are banning the EU countries. Would you please explain your decision to our readers?
Gangolf: This is a long story. I am unemployed since 2004, after I left Korbinian Strimmers group at the University of Munich. He shortened my salary every few months until it was not acceptable by me any more. Three years earlier I left Arndt von Haeseler’s Group at the Max-Planck-Institute for Evolutionary Anthropology in Leipzig, mainly also because of the miserable salary I got there.
When I was unemployed, I continued developing my Treefinder program, and Treefinder became more and more popular. I expected that someone would offer me a decently paid position for continuing my work, preferably at my then home place Munich, given that Treefinder was quite popular – but nobody did. Every possible employer I asked was only interested in his or her own project, not in supporting mine. Moreover, everyone would have at most paid me the same miserable salary.
So, I started my protest against the academic system, because it denies young researchers a reasonable long-term income at their respective home places, something that enabled them to escape from paying rent and buy a home and raise a family. Instead, the system invites immigrant scientists to keep the institutes full and the salaries low. I had severe doubts. I sent thousands of emails to members of the academic system in which I criticized them – and Treefinder became the counter-example in my campaign: look, an unemployed young researcher without a PhD title can do better than all of you well-paid professors, and better than all of the immigrant programmers you hired. Your system must be wrong! – This was my true motivation to make Treefinder the best program available, and I put a huge effort into that.
At least initially I thought it was that simple – namely that the academic system was simply too chintzy and promoted all of this mobility of scientists only to keep the salaries low. But then I read in the internet, in the alternative media, that the European countries were being controlled or at least strongly influenced by the USA, and that the USA were pursuing a not so well-known globalization plan. Globalization, in their view, means americanisation, the destabilzation of competing powers, and the creation of a global profitable new society. They want to rule and exploit the whole world. More precisely, a small elite in the USA wants to, not the American people. The promotion of world-wide migration is part of their plan. They even start wars just to generate enough migration. They are trying to destroy the world’s nations, because nations would defend themselves against foreign rulers. A world of migrants, on the other hand, would not care much who ruled. And this is not a conspiracy theory, it is written in books by leading US-ideologists, e.g. Barnett, Brzezinski. Especially in those books that must not be translated into foreign languages. See also:
The Americanized world that USA is trying to establish would be very bad for me. I do not want to be ruled by them, I do not want to migrate. I do not want to be ‘profitable’. So I declared sanction against the USA and certain EU countries.
Besides the academic system does not deserve to use my software, because it has not supported me.
3. Do you generally agree with Kai Kupferschmidt’s reporting in Science magazine – “Scientist says researchers in immigrant-friendly nations can’t use his software” published in Science about your decision (http://news.sciencemag.org/europe/2015/09/scientist-revokes-software-license-protest-immigration-friendly-policies)?
Gangolf: Kai’s article is very biased. A first version of his article contained several lies about me and my work, which unfortunately had been copied by others and then spread in the internet before I managed to get the lies removed. I am sure he did it deliberately. This is very bad journalism.
4. As it it is obvious to anyone with a functioning brain, the Americans created mess all around the Middle East and are asking the Europeans to suffer from it. Why aren’t the academics standing behind you then? For example, the Science article linked above quoted Sandra Baldauf of Sweden saying – “I’d say not being able to use Treefinder would be no great loss to anyone”. Based on what I read, Sweden is a mess due to refugee problem (http://www.acting-man.com/?p=40183).
Gangolf: Academics are being selected by the system for fitting into the system.
A recent job offer on evoldir contained the following: ” … We seek candidates who embrace and reflect diversity in the broadest sense. … “. That clearly excludes people like me.
Public opinion world-wide is strongly being influenced by the powerful elite, mostly from and through the USA:
I should mention that by far not all scientists are against me. I have received numerous emails congratulating me for the license change.
5. Linh Dinh maintains an excellent photojournalism blog showing pictures of collapse of USA. A few days back, he wrote this about the refugee crisis in Germany and Europe, and it appears to be more honest assessment than the mainstream media. What are your thoughts on it?
Gangolf: I haven’t read it. Maybe tomorrow.
6. What are your thoughts on European sanctions against Russia, as forced by US government?
Gangolf: European governments are being controlled or influenced by the USA.
This man, Egon Bahr, a former senior member of the German government, has admitted that:
Yesterday the French sites searched for Nobel prize, but nobody seems to care today. Even the Canadian internet sites are not bragging about a Canadian physicist winning the award. That is very good news for physics, because the lack of public interest will allow scientists to work without political and social noise.
University of Tokyo, Kashiwa, Japan
Arthur B. McDonald
Sudbury Neutrino Observatory Collaboration
Queen’s University, Kingston, Canada
Metamorphosis in the particle world
The Nobel Prize in Physics 2015 recognises Takaaki Kajita in Japan and Arthur B. McDonald in Canada, for their key contributions to the experiments which demonstrated that neutrinos change identities. This metamorphosis requires that neutrinos have mass. The discovery has changed our understanding of the innermost workings of matter and can prove crucial to our view of the universe.
Around the turn of the millennium, Takaaki Kajita presented the discovery that neutrinos from the atmosphere switch between two identities on their way to the Super-Kamiokande detector in Japan.
Meanwhile, the research group in Canada led by
Arthur B. McDonald could demonstrate that the neutrinos from the Sun were not disappearing on their way to Earth. Instead they were captured with a different identity when arriving to the Sudbury Neutrino Observatory.
A neutrino puzzle that physicists had wrestled with for decades had been resolved. Compared to theoretical calculations of the number of neutrinos, up to two thirds of the neutrinos were missing in measurements performed on Earth. Now, the two experiments discovered that the neutrinos had changed identities.
The discovery led to the far-reaching conclusion that neutrinos, which for a long time were considered massless, must have some mass, however small.
For particle physics this was a historic discovery. Its Standard Model of the innermost workings of matter had been incredibly successful, having resisted all experimental challenges for more than twenty years. However, as it requires neutrinos to be massless, the new observations had clearly showed that the Standard Model cannot be the complete theory of the fundamental constituents of the universe.
The discovery rewarded with this year’s Nobel Prize in Physics have yielded crucial insights into the all but hidden world of neutrinos. After photons, the particles of light, neutrinos are the most numerous in the entire cosmos. The Earth is constantly bombarded by them.
Many neutrinos are created in reactions between cosmic radiation and the Earth’s atmosphere. Others are produced in nuclear reactions inside the Sun. Thousands of billions of neutrinos are streaming through our bodies each second. Hardly anything can stop them passing; neutrinos are nature’s most elusive elementary particles.
Now the experiments continue and intense activity is underway worldwide in order to capture neutrinos and examine their properties. New discoveries about their deepest secrets are expected to change our current understanding of the history, structure and future fate of the universe.
Over the last few days, an obnoxious battle was taking place in US social media, where many scientists came to believe that Nobel prize in medicine would go to either the human genome sequencing project or CRISPR/cas9 and were fighting about who should be among the victorious three. After all, what other important contribution had been made by any other member of humanity?
They would be shocked to find out that the discoveries of real cures won this year’s award. The first of the cures was known as Mao’s secret malaria drug and was discovered at the height of Vietnam war. It was derived from Chinese ancient herbal medicine.
In 1967, a plant screening research program, under the name Project 523, was set up by the Chinese army to find an adequate treatment for malaria; the program and early clinical work were ordered of Chairman Mao Zedong at the request of North Vietnamese leaders to provide assistance for their malaria-ridden army. In the course of this research, Tu Youyou discovered artemisinin in the leaves of Artemisia annua (annual wormwood; 1972). The drug is named Qinghaosu in Chinese. It was one of many candidates tested as possible treatments for malaria by Chinese scientists, from a list of nearly 5000 traditional Chinese medicines. Tu Youyou also discovered that a low-temperature extraction process could be used to isolate an effective antimalarial substance from the plant; Tu says she was influenced by a traditional Chinese herbal medicine source “The Handbook of Prescriptions for Emergency Treatments” written in 340 BC by Ge Hong saying that this herb should be steeped in cold water.This book contained the useful reference to the herb: “A handful of qinghao immersed with two litres of water, wring out the juice and drink it all.” Tu’s team subsequently isolated a useful extract. The extracted substance, once subject to purification, proved to be useful starting point to obtain purified artemisinin.
Until recently, though, the drug’s origins were a mystery.
“I was at a meeting in Shanghai in 2005 with all of the Chinese malariologists and I asked who discovered artemisinin,” says Louis Miller, a malaria researcher at the US National Institutes of Health in Rockville, Maryland. “I was shocked that no one knew.”
Miller and his NIH colleage Xinzhuan Su began digging into the drug’s history. After reviewing letters, researchers’ original notebooks and transcripts from once-secret meetings, they concluded the major credit should go to pharmacologist Tu Youyou.
Her findings were published anonymously, and it was not until 2005, when a visiting researcher asked who had actually discovered artemisinin, that her name came to light — and even that required no small amount of research on the part of the medical community. A 2007 interview showed her living in poor conditions, working out of an old apartment building with intermittent heating problems. She only owned two electronic appliances: a telephone and a refrigerator (which she used to store herb samples).
William C. Campbell and Satoshi Omura won for developing a new drug, Avermectin, which has radically lowered the incidence of river blindness and lymphatic filariasis, or elephantiasis.
Parasitic worms, which cause river blindness and lymphatic filariasis, among other diseases, afflict a third of the world’s population, particularly in sub-Saharan Africa, South Asia and Latin America.
Dr. Omura, a microbiologist, focused on a group of bacteria, Streptomyces, that live in the soil and produce antibacterial agents. Dr. Omura isolated new strains of Streptomyces from soil samples and cultured them in the laboratory. From thousands of cultures, he selected about 50 of the most promising ones. One later turned out to be Streptomyces avermitilis, the source of Avermectin.
Dr. Campbell, an expert in parasite biology, showed that a component from one of Dr. Omura’s Streptomyces cultures was remarkably efficient against parasites in domestic and farm animals. This bioactive agent was purified and named Avermectin, which was subsequently chemically modified to a more effective compound called Ivermectin, that effectively killed parasitic larvae in humans. “Collectively, Omura and Campbell’s contributions led to the discovery of a new class of drugs with extraordinary efficacy against parasitic diseases,” the committee said.
A rather bizarre bioinformatics paper showed up in F1000. It made complete mockery of scientific publication standards with the excuse of ‘doing something new’. The paper has over 50 authors, and some are included for doing less than minor tasks. For example, one author only added two slashes to turn ‘http:contributor-covenant.org’ into ‘http://contributor-covenant.org’. That surely appears like a major contribution. Another author corrected only a typo in the code (changed ‘activae’ to ‘activate’).
It is also not clear, whether authors are listed twice or more in the authors’ list, because some names are included as pseudonyms (e.g. ‘en zyme’). Apparently the senior author gave more importance to github ID than real name. Berkeley Professor Lior Pachter’s attempt to sort that out had been met with very rude protest from the senior author of the F1000 paper. Pachter wrote in the comment section –
I noticed that “en zyme” is listed as an author with the affiliation of “independent Researcher in Boston, MA”. This individual appears to be Nathan Kohn, a part time lecturer at Boston University Metropolitan College and should be listed as such (assuming his contribution merits authorship).
The senior author of the paper replied in his blog –
Please note that there is a special place in hell reserved for people who attempt to deanonymize someone’s pseudonym on a whim; this is both unprofessional and potentially harmful to the individual in question. Yes, I’m talking to you, Lior.
That kind of rude response was definitely uncalled for, given that Pachter was making a very valid point (in fact two, because he also pointed out negligible contributions of authors).
When it comes to using pseudonyms for publishing paper, people often mention Gosset’s taking the name ‘Student’ to publish his famous paper on t-test. Wiki says –
The Student’s t-test work was submitted to and accepted in the journal Biometrika and published in 1908. Company policy at Guinness forbade its chemists from publishing their findings, so Gosset published his statistical work under the pseudonym “Student”.
What that example proves in the current context is anyone’s guess. If one looks into history, one can definitely find exceptions of all kinds – famous professor not giving credit to student, student stealing research results from professor and later becoming famous, people publishing research results based on what they overheard from others in conferences, and so on. Does that mean all those actions are justified, because someone well-known did before? Looks like even the author(s) of the wiki page is apologetic about Gosset’s apparently harmless deed and added a poor ‘mea culpa’ to explain that Gosset was not cheating his company –
Guinness had a policy of allowing technical staff leave for study (so-called “study leave”), which Gosset used during the first two terms of the 1906–1907 academic year in Professor Karl Pearson’s Biometric Laboratory at University College London. Gosset’s identity was then known to fellow statisticians and to editor-in-chief Karl Pearson. It is not clear how much of the work Gosset performed while he was at Guinness and how much was done when he was on study leave at University College London.
A better argument would be discussing the merits and demerits of using pseudonyms for scientific papers, and as demerits, we can see many. Someone can cheat his university or company out of legitimate intellectual property rights. Someone can take two pseudonyms to argue in favor of or against a controversial scientific argument, and appear victorious no matter which side wins. Imagine Dr. Jekyll supporting Darwin’s theory of evolution in late 19th century and Mr. Hyde writing papers it. However, having that kind of intelligent discussion does not seem appropriate for the F1000 paper, given that anyone who can fog a mirror has been made an author.
The senior author thinks his case is unusual, because he is publishing a paper on a software. A software is already a copyrighted publication by itself, and the only reasons another paper needs to announce its arrival are (a) present unique algorithmic contribution, (b) make grant Gods, who give more importance to papers than computer programs, happy. In the first case, 50 people rarely create an algorithm and I doubt that is the case here. Speaking of the second case, this mockery of science has been funded by NHGRI, which is a mockery of science by itself.
Pachter has taken a courageous stand given the risk of pointing out discrepancies in a paper with 50 authors and annoying many of them. I am puzzled the other authors allowed this nonsense to take place in their name.
The most puzzling observation one can make from the paper is the discrepancy between the claimed and the actual error rate of nanopore sequences. We recently had this discussion with David Eccles, who wrote in the comment section – “The median error per base was approximately 7% for this run (i.e. 93% accuracy)”. Similar claims of 92%-93% accuracy had been made by other Nanopore promoters. If that is true, the obvious follow-up question would be – why does Mick Watson (and many others) need to use Illumina reads to assemble bacterial genomes? For Pacbio reads with 85% accuracy, one can easily assemble bacterial genomes from Pacbio-only.
The answer lies in two ‘details’. (i) For Pacbio reads, 85% accuracy is before processing, whereas Oxford nanopore reads appear to go through rounds of processing to get to 92%. I pointed that out to David Eccles in the comment section. (ii) The second and more important point is that the error distribution of Pacbio reads is completely random, thus making compensation through high coverage possible. We are not sure what the error distribution of Oxford nanopore reads is. It is possibly not random given that they continue to need support from Illumina sequences for genome assembly.
The hybrid assembly argument vouched in the following abstract was the status quo for Pacbio one year back, but based on my recent conversation with the members of Pacbio community, those researchers are increasingly moving away from using any Illumina read. Apparently, those short reads seem to complicate the assembly process instead of helping. They were useful, when Pacbio reads were expensive, but will not be any more.
Second and third generation sequencing technologies have revolutionised bacterial genomics. Short-read Illumina reads result in cheap but fragmented assemblies, whereas longer reads are more expensive but result in more complete genomes. The Oxford Nanopore MinION device is a revolutionary mobile sequencer that can produce thousands of long, single molecule reads. Results
We sequenced Bacteroides fragilis strain BE1 using both the Illumina MiSeq and Oxford Nanopore MinION platforms. We were able to assemble a single chromosome of 5.18 Mb, with no gaps, using publicly available software and commodity computing hardware. We identified gene rearrangements and the state of invertible promoters in the strain. Conclusions
The single chromosome assembly of Bacteroides fragilis strain BE1 was achieved using only modest amounts of data, publicly available software and commodity computing hardware. This combination of technologies offers the possibility of ultra-cheap, high quality, finished bacterial genomes.
Sam Minot pointed out Jared Simpson’s work on E. coli assembly from Oxford nanopore only, which we covered here-
It is puzzling that despite that earlier success, others are not adopting similar approach, given that assembling from Oxford nanopore only would be the biggest selling point for the company. It does not make sense to talk about carrying USB-sized sequencer to the field, if one also has to carry a large Illumina instrument. There are two possible explanations for Mick Watson’s not using Simpson’s algorithm/program – (i) he is not aware of it, (ii) he is unable to make it work.
[Short explanation: large number of investors are betting on all kinds of outcomes based on available news (such as PacBio Mini?), and the above ratio charts are condensed versions of their expectations over the last two years. As it appears, those investors are at a crossroad. If the chart breaks above triangle, long noisy reads have better ‘expected’ future. (Edit. added linear scale chart, which is more appropriate for ratios).