Test your irony meter

The irony meter was a running joke on the newsgroup talk.origins back in the last century. Our irony meters were supposed to protect us from the craziness of creationists but as soon as we built a really good irony meter a new bit of creationist crazy came along and fried it. Apparently Jesus and Mo have the same problem.

Scientists fight back against fake news and pseudoscience

You probably know that climate change is real and humans are a major cause of global warming. You probably know that life has evolved and the Biblical story of creation is false. Scientists have been actively promoting these ideas for decades and they've been relatively successful in most countries. What you may not know is that these are just two of the many controversial claims that scientists are fighting. You may even have been tricked into believing some of the other pseudoscientific claims that are out there.

Do you think genetically-modified organisms are dangerous? Do you think vaccines are a threat to your child's well-being? Do you consult a naturopath or a homeopath? How about a chiropracter? Do you take daily vitamin supplements? Do you avoid gluten or lactose? Do you think hamburgers and fries are unhealthy? Poutine? Have you ever had acupuncture? Have you ever been detoxified? Are you afraid of free radicals? Is Round-Up a deadly poison? Do you spend extra money buying "organic" food? Are you afraid of fluoride? Are preservatives always bad? Is Diet Coke gonna kill you? Do skinny people live longer? Are whole wheat bagels better for you than the regular kind? Do you take probiotics? Do you even know what they are? Can you avoid cancer by eating healthy and working out every day?1

If you answered "yes" to any of those questions then chances are you've fallen for some fake science. It's more common than you might think. I have many friends who take vitamin supplements, for example, in spite of the fact there's no scientific evidence that they do any good. They've been sucked in by the fake "health" food industry who are more than willing to take your money. Last year the so-called "health and wellness" industry raked in a trillion dollars [Health and Wellness the Trillion Dollar Industry in 2017].

Fortunately, there are a few scientists out there who are fighting back and, even more importantly, the legitimate press is beginning to pay attention. This is important because those scientists are fighting a trillion dollar industry and they're mostly doing it for free. Today I was pleased to read the following article in Toronto Star: Scientists, researchers fight against online plague of nutrition pseudoscience.
This group is collectively working to debunk the most egregious health myths with evidence-based, factual information.
It always a good thing when proponents of evidence-based facts get as much attention as the proponents of pseudoscience. One of the scientists highlighted in the article is Timothy Caulfield, a professor at the University of Alberta Health Law Institute. He's the author of Is Gwyneth Paltrow Wrong About Everything? (Spoiler Alert! - the answer is "yes.")
Finding health information online is easy. Cutting through the clutter and getting facts is very difficult. There’s a cacophony of voices, each saying something different. The confusion worsens when charlatans provide false hope and bad advice.

But there is a glimmer of hope. Scientists and researchers are working to debunk the most egregious health myths and educate readers with evidence-based, factual information. Let’s call them skeptics, myth-busters or debunkers. In any case, this group is collectively using science to fight back against the pseudoscience (such as fad diets and quack cancer cures).
It's fun to debunk the claims of pseudoscience but let's not forget that the important goal is to teach critical thinking in our schools so that our children grow up armed with the tools to avoid falling for false claims in the first place.

1. If I haven't found at least one question that makes you want to post an angry rebuttal then please let me know and I will add some others.

Dirty bacteria

Did you know that the dirt in your local park is full of bacteria? Each scoop of soil contains millions of bacteria. And it's not just in your local park, soil bacteria are everywhere. This is part of the reason why the total mass of bacteria on the planet outweighs all of the eukayotes combined, including elephants and whales.

There are hundreds of different species of bacteria in your local dirt. They are as different from each other as moose and mushrooms.

Did you ever wonder whether the bacteria in Australian soil are similar to the bacteria in Austrian soil? Delgado-Baquerizo and his colleagues did, so they tested soils from all over the world. The results are published in a recent issue of Science (Delgado-Baquerizo et al., 2018).

The answer is yes ... and no. They looked at 237 locations on all continents except Antarctica. Most samples had about 1000 different species—the authors call them "phylotypes" because it's hard to define what a species is in bacteria. Only a small number of species (phylotypes) were found in all locations (511 out of 25,224 = 2%) but they accounted for almost half of the total mass. Here's how the authors describe their result ...
Together, our results suggest that soil bacterial communities, like plant communities, are typically dominated by a relatively small subset of phylotypes.
Most of those 511 dominant phylotypes fall into two large and diverse clades (phyla?): Proteobacteria and Actinobacteria. The distribution is shown in Figure 1 of the paper (left). It illustrates a little-known fact about bacteria; namely, that they are a very diverse group. Scientists are only beginning to explore this diversity. Only 18% of the 511 dominant phylotypes were previously known to science!

Image Credit: Bacillus Sp. soil bacteria from The ecology of soil-borne human diseases

Delgado-Baquerizo, M., Oliverio, A.M., Brewer, T.E., Benavent-González, A., Eldridge, D.J., Bardgett, R.D., Maestre, F.T., Singh, B.K., and Fierer, N. (2018) A global atlas of the dominant bacteria found in soil. Science, 359(6373), 320-325. doi: doi: 10.1126/science.aap9516

Happy Darwin Day 2018!

Charles Darwin, the greatest scientist who ever lived, was born on this day in 1809 [Darwin still spurs tributes, debates] [Happy Darwin Day!] [Darwin Day 2017]. Darwin is mostly famous for two things: (1) he described and documented the evidence for evolution and common descent and (2) he provided a plausible scientific explanation of evolution—the theory of natural selection. He put all this in a book, The Origin of Species by Means of Natural Selection published in 1859—a book that spurred a revolution in our understanding of the natural world.

Modern evolutionary theory has advanced well beyond Darwin's theory but he still deserves to be honored for being the first to explain evolution and promote it in a way that convinced others. Here's one passage from the introduction to Origin of Species.
Although much remains obscure, and will long remain obscure, I can entertain no doubt, after the most deliberate and dispassionate study of which I am capable, that the view which most naturalists entertain, and which I formerly entertained—namely, that each species has been independently created—is erroneous. I am fully convinced that species are not immutable; but that those belonging to what are called the same genera are lineal descendants of some other and generally extinct species, in the same manner as the acknowledged varieties of any one species are the descendants of that species. Furthermore, I am convinced that Natural Selection has been the main but not exclusive means of modification.

One philosopher’s view of random genetic drift

Random genetic drift is the process whereby some allele frequencies change in a population by chance alone. The alleles are not being fixed or eliminated by natural selection. Most of the alleles affected by drift are neutral or nearly neutral with respect to selection. Some are deleterious, in which case they may be accidentally fixed in spite of being selected against. Modern evolutionary theory incorporates random genetic drift as part of population genetics and modern textbooks contain extensive discussions of drift and the influence of population size. The scientific literature has focused recently on the Drift-Barrier Hypothesis, which emphasizes random genetic drift [Learning about modern evolutionary theory: the drift-barrier hypothesis].

Most of the alleles that become fixed in a population are fixed by random genetic drift and not by natural selection. Thus, in a very real sense, drift is the dominant mechanism of evolution. This is especially true in species with large genomes full of junk DNA (like humans) since the majority of alleles occur in junk DNA where they are, by definition, neutral.1 All of the data documenting drift and confirming its importance was discovered by scientists. All of the hypotheses and theories of modern evolution were, and are, developed by scientists.

Nothing in biology makes sense except in the light of population genetics.

Michael Lynch
You might be wondering why I bother to state the obvious; after all, this is the 21st century and everyone who knows about evolution should know about random genetic drift. Well, as it turns out, there are some people who continue to make silly statements about evolution and I need to set the record straight.

One of those people is Massimo Pigliucci, a former scientist who's currently more interested in the philosophy of science. We've encountered him before on Sandwalk [Massimo Pigliucci tries to defend accommodationism (again): result is predictable] [Does Philosophy Generate Knowledge?] [Proponents of the Extended Evolutionary Synthesis (EES) explain their logic using the Central Dogma as an example]. I looks like Pigliucci doesn't have a firm grip on modern evolutionary theory.

His main beef isn't with evolutionary biology. He's mostly upset about the fact that science as a way of knowing is extraordinarily successful whereas philosophy isn't producing many results. He loves to attack any scientist who points out this obvious fact. He accuses them of "scientism" as though that's all it takes to make up for the lack of success of philosophy. His latest rant appears on the Blog of the American Philosophers Association: The Problem with Scientism.

I'm not going to deal with the main part of his article because it's already been covered many times. However, there was one part that caught my eye. That's the part where he lists questions that science (supposedly) can't answer. The list is interesting. Pigliucci says,
Next to last, comes an attitude that seeks to deploy science to answer questions beyond its scope. It seems to me that it is exceedingly easy to come up with questions that either science is wholly unequipped to answer, or for which it can at best provide a (welcome!) degree of relevant background knowledge. I will leave it to colleagues in other disciplines to arrive at their own list, but as far as philosophy is concerned, the following list is just a start:
  • In metaphysics: what is a cause?
  • In logic: is modus ponens a type of valid inference?
  • In epistemology: is knowledge “justified true belief”?
  • In ethics: is abortion permissible once the fetus begins to feel pain?
  • In aesthetics: is there a meaningful difference between Mill’s “low” and “high” pleasures?
  • In philosophy of science: what role does genetic drift play in the logical structure of evolutionary theory?
  • In philosophy of mathematics: what is the ontological status of mathematical objects, such as numbers?
[my emphasis LAM]
Before getting to random genetic drift, I'll just note that my main problem with Pigliucci's argument is that there are other definitions of science that render his discussion meaningless. For example, I prefer the broad definition of science—the one that encompasses several of the Pigliucci's questions [Alan Sokal explains the scientific worldview][Territorial demarcation and the meaning of science]. The second point is that no matter how you define knowledge, philosophers haven't been very successful at adding to our knowledge base. They're good at questions (see above) but not so good at answers. Thus, it's reasonable to claim that science (broad definition) is the only proven method of acquiring knowledge. If that's scientism then I think it's a good working hypothesis.

Now back to random genetic drift. Did you notice that one of the questions that science is "wholly unequiped" to answer is the following: "what role does genetic drift play in the logical structure of evolutionary theory?" Really?

Pigliucci goes on to explain what he means ...
The scientific literature on all the above is basically non-existent, while the philosophical one is huge. None of the above questions admits of answers arising from systematic observations or experiments. While empirical notions may be relevant to some of them (e.g., the one on abortion), it is philosophical arguments that provide the suitable approach.
I hardly know what to say.

How many of you believe that the following statements are true with respect to random genetic drift and evolutionary theory?
  1. The scientific literature on all the above is basically non-existent.
  2. The philosophical literature is huge.
  3. The question does not admit of answers arising from systematic observations or experiments.
  4. It is philosophical arguments that provide the suitable approach.

1. There are some very rare exceptions where a mutation in junk DNA may have detrimental effects.

We live in the age of bacteria

I'm sad because we now have almost a whole generation of young people who know very little about Stephen Jay Gould. (He died of cancer in 2002.) I was thinking of this yesterday as I was preparing a post on bacteria. Gould's 1996 book, Full House, is about fundamental misconceptions of evolution and progress and it contains the following passage (p. 176) ...

We live now in the "Age of Bacteria." Our planet has always been in the "Age of Bacteria," ever since the first fossils—bacteria, of course—were entombed in rocks more than three and a half billion years ago.

On any possible, reasonable, or fair criterion, bacteria are—and always have been—the dominant forms of life on earth.
Listen to him make this point twenty years ago ...

Junior scientist snowflakes

A recent letter in Nature draws attention to a serious (?) problem in modern society; namely, the persecution of junior scientists by older scientists who ask them tough questions. Anand Kumar Sharma warns us: "Don’t belittle junior researchers in meetings". Here's what he says, ...

The most interesting part of a scientific seminar, colloquium or conference for me is the question and answer session. However, I find it upsetting to witness the unnecessarily hard time that is increasingly given to junior presenters at such meetings. As inquisitive scientists, we do not have the right to undermine or denigrate the efforts of fellow researchers — even when their reply is unconvincing.

It is our responsibility to nurture upcoming researchers. Firing at a speaker from the front row is unlikely to enhance discussions. In my experience, it is more productive to offer positive queries and suggestions, and save negative feedback for more-private settings.
I wasn't going to comment on this but Neuroskeptic blogged about it and supported the idea that junior scientists need special protection when they present their work at meetings and conferences [Hostile Questions at Scientific Meetings]. He says,
In my view, a conference is not a place to be making critical comments. For one thing, it is very difficult to critically appraise a conference presentation, because they don’t provide the full details of the study. It is also unlikely that putting a presenter on the spot with a hard question is going to elicit a useful answer. It’s better to wait until the paper is published, and then critique that, giving the authors time to respond properly.
I recognize that there are abuses from time to time but I take the opposite position. I don't think there's enough harsh criticism at scientific meetings. I think that too many scientists get away with making ridiculous claims that go unchallenged out of politeness and political correctness. I think we need MORE hostile questions not fewer. Why should a scientist be allowed to make stupid statements at a conference presentation on the grounds that they can't be criticized because the work isn't published?

Should we treat junior scientists any differently than senior scientists? Should we allow junior scientists the privilege of saying stupid things without being challenged as long as they are under 40 years old? Let's hear from some younger scientists 'cause I'm pretty sure that all of us old curmudgeons don't hold back from criticizing our younger colleagues.

When I was younger—yes, that's me on the left—I would have been insulted to be told that I was being treated as a child, not an equal, by my senior colleagues.

Are splice variants functional or noise?

This is a post about alternative splicing. I've avoided using that term in the title because it's very misleading. Alternative splicing produces a number of different products (RNA or protein) from a single intron-containing gene. The phenomenon has been known for 35 years and there are quite a few very well-studied examples, including several where all of the splice regulatory factors have been characterized.

The number of known examples is quite small in any given species. In contrast, the number of different splice variants is enormous. Most human genes, for example, are associated with a dozen or so different variants that have been detected over the years. Almost of of these splice variants have been rejected by genome annotators because they are very rare, never leave the nucleus, and are never present in sufficient quantities to be functional. They are undoubtedly junk RNA produced by the sloppy spliceosome. This kind of noise should not be called alternative splicing because that term should be restricted to real examples that produce functional variants by some sort of regulatory mechanism.

This seems like common sense to me but, unfortunately, most scientists disagree. They continue to refer to any example of splice variants as alternative splicing even though they might be just splicing errors. In fact, most of these scientists don't even consider the possibility of splicing errors. See the following posts for a more thorough discussion of this problem.

Debating alternative splicing (part I)
Debating alternative splicing (part II)
Debating alternative splicing (Part III)
Debating alternative splicing (Part IV)

A recent paper by John Mattick and his collaborators highlights the problem (Deveson et al., 2017). Recall that Mattick is a prominent opponent of junk DNA. He thinks that most of the genome is devoted to producing regulatory RNAs. His "proof" is pervasive transciption. He claims there are thousands and thousands on long nocoding RNAs that have a function [John Mattick still claims that most lncRNAs are functional].

His most recent paper employs the latest technology for detecting RNAs in a cell. The authors highlight the fact that they can detect very low abundance RNAs. They apply the technique to map all the RNAS complementary to the DNA on human chromosome 21. They choose three tissues; testis, brain, and kidney. Two of these tissues are well-known examples of noisy transcription.

The results are not unexpected. They detected an enormous number of different transcripts covering most of the non-repetitive DNA in chromosome 21. Each protein-coding gene matched to dozens of different splice variants in addition to the standard mRNA. Although the authors make passing reference to the controversy over splicing, it's clear that they treat all of these mRNA variants as examples of true alternative splicing. But that's not the main point of their paper. The main point is that the rest of the chromosome specifies a large number of noncoding RNAs and those RNAs exhibit an enormous diversity of splice variants. The result is nicely captured in their summary image (right).

The old RNA-Seq view is shown in the upper-right part of the image. A typical protein-coding gene produces a number of splice variants that I assume are examples of splicing errors. Mattick and his colleagues assume they are due to alternative splicing. The noncoding part of the genome is complementary to another set of transcipts with a limited set of splice variants. Mattick assumes these regions are genes and the RNAs are functional, although he has no proof of that. I assume that most of these RNA are spurious transcipts of junk DNA. This should be the default assumption.

The new view is derived from their more exhaustive analysis of very rare transcripts. There are more splice variants from protein-coding genes but the increase is not enormous. In contrast, there are many more variants RNAs from the rest of the genome and this includes an enormous diversity of different exons. The title of the paper say it all: Universal alternative splicing of noncoding exons. Here are the main conclusion of the paper ...
We propose that noncoding exons are functionally modular, with alternative splicing generating an enormous repetoire of potentially regulatory RNAs and a rich transcriptional reservoir for gene evolution. (abstract)

One can envision a scenario where individual noncoding exons interact independently with other biomolecules (proteins, RNAs and/or DNA-motifs), organizing these around the scaffold of a noncoding transcript. In this way, alternative isoforms could assemble different collections of binding partners to dynamically regulate cellular processes. (discussion)
Yes, it's true that one could envisage such a scenario. One can image many things, but the real question is not how potent your imagination is but whether it's realistic.

Scenarios should be based on facts and not on wishful thinking. In this case there's a lot of evidence that most of our genome is junk. If you are going to propose that most of it contains genes for regulatory RNAs then you have an obligation to refute or discredit the evidence for junk. This paper doesn't do that.

Similarly, there are many good reasons to suspect that splice variants are mistakes in splicing. The variants are not conserved, most are present at less than one copy per cell, splicing errors are known to occur at relatively high frequency, and very few have been shown to have a function. The default assumption must be that they are junk RNA unless proven otherwise.

Mattick and his colleagues dismiss some of these objections using arguments that make no sense. The problem with this paper is that it is promoting an extraordinary claim without any serious evidence of function, let alone extraordinary evidence. I don't understand how it passed peer review. The data may be fine but the interpretation and the conclusions are not.

I think the tide is turning against Mattick and his supporters but perhaps that's just wishful thinking on my part. Take a look at the RNA variants in the lower right-hand corner of the figure. How many of you believe they represent exquisite fine-tuning of a regulatory RNA? How many of you think they are mostly transcriptional and splicing errors?

Deveson, I.W., Brunck, M.E., Blackburn, J., Tseng, E., Hon, T., Clark, T.A., Clark, M.B., Crawford, J., Dinger, M.E., Nielsen, L.K., Mattick, J.S., and Mercer, T.R. (2017) Universal alternative splicing of noncoding exons. Cell Systems, 6:(1-11). [doi: 10.1016/j.cels.2017.12.005]

The Salzburg sixty discuss a new paradigm in genetic variation

Sixty evolutionary biologists are going to meet next July in Salzburg (Austria)to discuss "a new paradigmatic understanding of genetic novelty" [Evolution – Genetic Novelty/Genomic Variations by RNA Networks and Viruses]. You probably didn't know that a new paradigm is necessary. That's because you didn't know that the old paradigm of random mutations can't explain genetic diversity. (Not!) Here's how the symposium organizers explain it on their website ...

For more than half a century it has been accepted that new genetic information is mostly derived from random‚ error-based’ events. Now it is recognized that errors cannot explain genetic novelty and complexity.

Empirical evidence establishes the crucial role of non-random genetic content editors such as viruses and RNA-networks to create genetic novelty, complex regulatory control, inheritance vectors, genetic identity, immunity, new sequence space, evolution of complex organisms and evolutionary transitions....

This new empirically based perspective on the evolution of genetic novelty will have more explanatory power in the future than the "error-replication" narrative of the last century.
Wow! Who knew?

The lead organizer is Günther Witzany, a philosopher of science and a prominent member of The Third Way [The Third Way: Günther Witzany]. We've encountered him before on Sandwalk: Here's why you can ignore Günther Witzany. Just about anyone can misunderstand molecular biology but it takes a philosopher of science to really screw it up. Witzany says ...
The older concepts we have now for a half century cannot sufficiently explain the complex tendency of the genetic code. They can't explain the functions of mobile genetic elements and the endogenous retroviruses and non-coding RNAs. Also, the central dogma of molecular biology has been falsified -- that is, the way is always from DNA to RNA to proteins to anything else, or the other "dogmas," e.g., replication errors drive evolutionary genetic variation, that one gene codes for one protein and that non-coding DNA is junk. All these concepts that dominated science for half a century are falsified now. ...
Here's a summary of where my views differ ...
  1. The fundamental concepts in evolution and molecular biology were worked out in the middle of the last century and thery have been steadily improved and modified since then. They are fully capable of explaining mobile genetic elements, endogenous retroviruses, and non-coding RNAs. Read any textbook.
  2. The Central Dogma of Molecular Biology says that once information is transferred to protein it can't go back to nucleic acids [Central Dogma of Molecular Biology]. It's blatantly obvious that Günther Witzany doesn't understand the Central Dogma. It's obvious that he hasn't read Crick's papers.
  3. The idea that replication errors create genetic variation has not been falsified. It is by far the most important source of mutation.
  4. The idea that one gene codes for one protein is a false strawman version of our current understanding of a gene [What Is a Gene?]. No knowledgeable scientist ever thought that all genes produced proteins and no knowledgeable scientist since 1980 was unaware of genes encoding multiple proteins. Read a textbook.
  5. No knowledgeable scientist ever said that all non-coding DNA is junk. They do, however, say that most of the DNA in the human genome is junk. That's a concept that was formed in the middle of the last century and has become more and more true as evidence accumulates in the 21st century. It has not been falsified as Günther Witzany claims. He has not been keeping up with the scientific literature.
  6. Nobody is questioning the fact that transposons and viruses can cause mutations and genomic rearrangements. The only serious debate is over the frequency of such events. By looking at the amount of variation in individual humans, scientists have determined that 99.9% of all variation is in the form of single nucleotide changes (SNPs) or small (1-10 bp) insertions/deletions. Larger differences due to transposons and viral insertions/deletions account for only 0.1% of the total [Genetic variation in human populations]. All sorts of mutations will contribute to evolution in the long run but it's absurd to think there's any "paradigm shift" in the making. Instead, this is a classic example of a paradigm shaft (a term coined by Diogenes on an earlier Sandwalk post).

How many lncRNAs are functional?

There's solid evidence that 90% of your genome is junk. Most of it is transcribed at some time but the transcripts are transient and usually confined to the nucleus. They are junk RNA [Functional RNAs?]. This is the view held by many experts but you wouldn't know that from reading the scientific literature and the popular press. The opposition to junk DNA gets much more attention in both venues.

There are prominent voices expressing the view that most of the genome is devoted to producing functional RNAs required for regulating gene expression [John Mattick still claims that most lncRNAs are functional]. Most of these RNAs are long noncoding RNAs known as lncRNAs. Although most of them fail all reasonable criteria for function there are still those who maintain that tens of thousands of them are functional [How many lncRNAs are functional: can sequence comparisons tell us the answer?].

There are very few serious reviews that address the controversy over function (but see Palazzo and Lee, 2015 ... the figure is from their paper). That's why I want to highlight a review that's just been published in Cell. It's a review that recognizes the controversy over function and points to the possibility that most putative lncRNAs may be junk (Kopp and Mendell, 2018). I'm going to quote directly from the introduction and the conclusion to show you how scientific reviews are supposed to be written.
There is a broad range of estimates for the number of lncRNA genes in mammals, ranging from less than 20,000 to over 100,000 in humans. Nevertheless, the function and biological relevance of the vast majority of lncRNAs remain enigmatic. Given that transcriptional regulatory elements, such as enhancers and promoters, are now known to initiate transcription bi-directionally, it is likely that many lncRNAs—if not the majority—actually represent RNAs that initiate at enhancers or promoters but do not perform sequence-specific functions. This conclusion is further suggested by the fact that many lncRNAs are localized to the nucleus with low expression levels and little primary sequence conservation. Recent reports of local gene regulation by lncRNA loci reinforce this notion and suggest that in many cases, the act of transcription or DNA elements within the lncRNA locus are more likely to be the source of regulatory activity than the actual lncRNA itself. Given these observations, it is clear that the mere existence or production of an RNA does not automatically imply its functionality. Indeed, we must assume until proven otherwise that of the tens of thousands of annotated lncRNAs, those that function independently of the DNA sequence from which they are transcribed represent a small minority. Nevertheless, even if a small percentage of lncRNAs are functional, they would still constitute a major gene class with hundreds or possibly thousands of members.
The best available data shows that less than 500 putative lncRNAs have a well-defined function. When I'm calculating the amount of functional DNA in the human genome I usually assume 5,000 genes for noncoding RNAs—most of them are not lncRNAs. I still think that's a good estimate.

The act of transcription around promoter regions may play a role in regulation. In such cases, the sequence of the transcript may be irrelevant but the transcribed region of the genome has a function. There aren't very many proven examples of this type of function. In most cases it looks like the transcripts are just due to sloppy initiation. Kopp and Mendell make an important point in the introduction when they say that the mere existence of a transcript does not mean it has a function. This point is usually ignored in the scientific literature.

The authors reinforce this view in their conclusions. They emphasize a point that most scientists find awkward; namely, that the default assumption must be lack of function (junk RNA) and the burden of proof is on those who propose that most lncRNAs have a function. When we detect a transcript, the most we can say for certain is that there's a transcription initiation site nearby. It may or may not be important.
Over the last decade, the study of lncRNAs has stimulated vigorous debate over the question of whether noncoding RNAs represent “transcriptional noise” or truly functional biomolecules. Clearly, there is no unifying answer—meaningful understanding of lncRNA function (or lack thereof) can only be achieved from detailed study on a case-by-case basis. Importantly, our evolving understanding of the prevalence of genomic elements that produce noncoding transcripts, such as enhancers, has mandated that we approach the experimental evaluation of a lncRNA locus with an agnostic view regarding whether the produced RNA is functional. As Occam’s razor dictates, the simplest hypothesis, in this case that the production of a lncRNA most likely marks the presence of a regulatory DNA element, is often the correct one.
I'm pleased to see that more and more scientists are recognizing the very real controversies over junk DNA and the role of pervasive transcription. Unfortunately, it still takes a bit of courage to stand up to the dominant (but incorrect) paradigm promoted by the ENCODE publicity campaign over the past decade.

Kopp, F., and Mendell, J.T. (2018) Functional Classification and Experimental Dissection of Long Noncoding RNAs. Cell, 172:393-407. [doi: 10.1016/j.cell.2018.01.011]

Palazzo, A.F., and Lee, E.S. (2015) Non-coding RNA: what is functional and what is junk? Frontiers in Genetics, 6. [doi: 10.3389/fgene.2015.00002]