Mystery Rays from Outer Space

Meddling with things mankind is not meant to understand. Also, pictures of my kids

July 3rd, 2015

Adaptive hybridization

Can a hybrid between two species might have a selective advantage?  Although hybridization is usually a deleterious event, it doesn’t have to be. The example I usually use are Darwin’s Finches.

Hybridization between this species and two others resulted in gene exchange, but only after the El Nino when hybrid fitness was much enhanced under the altered feeding conditions. … hybrids were at a strong disadvantage before the 1982-1983 El Nino event, and at a small advantage afterwards.

Evolution of Darwin’s Finches Caused by a Rare Climatic Event

I recently learned about another example that’s even better.  Quoting Darren Naish from his Tetrapod Zoology blog:

do have to give honorary mention to the amazing discovery that the females of S. bombifrons will preferentially mate with the males of S. multiplicata where the two occur in sympatry, and where this sympatry involves shallow, rapidly drying pools. The conclusion from this discovery is that hybridisation is adaptive in S. bombifrons: that is, that females are able to give their offspring a survival advantage by hybridising with members of another species (Pfennig 2007).

North American spadefoot toads and their incredible fast-metamorphosing, polymorphic tadpoles | Tetrapod Zoology

The reference is to Karen Pfenning’s Facultative mate choice drives adaptive hybridization (full paper here, at least for now).

A review paper discussing interspecies hybridization in general (and Pfenning’s paper in particular) is Mating with the wrong species can be right (full-ltext link):

… interspecific hybridisation … is very unequally distributed among and within taxa, and in some animals the rate of hybridisation even exceeds that in plants [2–4]. This shifted the debate from a specific comparison between plants and animals to a more general question: what traits and environmental conditions separate groups with frequent and successful hybridisation from those where it does not occur in the first place (pre-zygotic isolation) or leads to unviable or less fertile offspring with no or little chance to pass on their genes (postzygotic isolation)?

July 1st, 2015

Why don’t I turn into a fish when I eat fish?

The question on Quora was:

Why don’t I turn into a fish when I eat fish? Or a cow when I eat beef?

The expanded explanation for the question was:

Before this is labelled as silly, here is explanation: there are specific chemicals in our bodies whose purpose is to prevent foreign genetic material in a body and cell from being read and translated into mRNA. What are the names of these chemicals and processes? How do they work?

My answer was:

Not a silly question at all, especially if we bypass the “eat” part and ask why just, say, injecting a fish cell into our arm wouldn’t turn us into a fish, or why giving our kid a transfusion of mongoose blood wouldn’t turn him into a speedy superpowered whizzer.

There are two parts to the answer.  First, DNA needs to have an elaborate support system before it can do anything.  It needs to be in a nucleus, wrapped in histones and other proteins, with access to polymerases and other enzymes, and so on and so on.  Just shoving DNA into your bloodstream doesn’t give it access to those things, so it can’t take over your cells to make fish or mongoose type proteins.

(But if you add to the DNA a system for entering a new cell and taking over the built-in systems, then you have a virus, which essentially does exactly that — turns your cells into a system for making more viruses.)

But why not a whole cell? Why can’t a fish cell settle down comfortably into our body and just pump out fish proteins all day long?

The answer is the immune system, which is aimed at identifying things that are not “self” — that is, that don’t match the template of our own cells — and to attack and reject them.  The immune system is very good at that, and can even reject very similar cells, like those of a different human, so identifying a fish or a mongoose cell is very easy to do, and those cells would be very quickly attacked and destroyed.

(Today, the immune system is tuned for identifying and destroying bacteria and viruses and so on.  But it’s possible that hundreds of millions of years ago, much of the immune system was tuned for exactly what we’re talking about here — preventing foreign cells from moving into the friendly environment and taking over.)

In response to a question in the comments (“What about plants and simpler organisms which don’t have complex immune systems?”), I added:

You have to get very “simple” in the simpler-organisms category before they lose the parts of the immune system that recognize different cell types, although the actual mechanisms are quite different in different organisms.

As for plants, they don’t reject foreign material, at least not in the same way that animals do; you can graft different plants, or even different species, together and they’ll grow pretty happily.  Grape vines and apple trees, to name just two, often have this done.

As to how, or even whether, plants reject a more subtle invasion by parasitic plants … I just don’t know.  Hopefully a botanist can answer.

 

June 24th, 2015

Are there any proteins that, when sequenced, have segments that spell English or colloquial words?

The question on Quora was:

Are there any proteins that, when sequenced, have segments that spell English or colloquial words?

My answer was:

A typical protein is about 350 amino acids long.  I am not aware of any English or colloquial words that are 350 letters long.  Very few, if any, functional proteins are less than 20 amino acids long, which is still very long for English words.

Many protein sequences contain within them English words and names. ELVIS can be found in many proteins, but ELVISISALIVE hasn’t turned up yet.  CRICK can be found in many,  FRANKLIN appears once in a hypothetical protein from Treponema primitia (WP_010253273) and of course WATSON is impossible.

What’s the longest English word that can be found in the GenBank protein collection? Offhand, I don’t know (and it will change on a regular basis, at the rate the collection is growing).  I bet I can find it in a few lines of code, though, and if no one beats me to it I’ll take a shot at it tomorrow; it’s too late tonight.

Update: The longest more or less English word I can find in the human reference sequence protein database is “TARGETEER”, 9 letters long.  It’s found in several isoforms of “C12orf42″, e.g. uncharacterized protein C12orf42 isoform 1 [Homo sapiens].

I only looked in the human reference sequence library, not the complete protein database for NCBI, which would have taken too long for download (too long for the mild curiosity I had, anyway).  This database has 72,204 protein sequences in it, with a total length of 46,315,661 amino acids; average protein length 636.4, median length 467.0, geometric mean length 468.5, distribution looking like this:

For words, I used the builtin unix dict (on my computer, /usr/share/dict/words), which contains 235,886 more or less English words ranging from 1 through 24 letters long (THYROPARATHYROIDECTOMIZE, TETRAIODOPHENOLPHTHALEIN, SCIENTIFICOPHILOSOPHICAL, PATHOLOGICOPSYCHOLOGICAL, and FORMALDEHYDESULPHOXYLATE, if you’re playing Scrabble).

“TARGETEER” was the 119,925th-longest word in the dictionary, and since I started with the longest and worked down it was over halfway through the dictionary (50.8%) before I got the first hit.  All in all, it took close to an hour to run in the background, with no attempt whatsoever at optimizing the script.

March 17th, 2014

Influenza subtypes in birds

What subtypes of influenza are found in birds?

Influenza is naturally a disease of wild waterfowl; humans, like dogs, chickens, and whales, are occasional victims of mutated viruses from this vast global reservoir of viruses.  In wild birds, flu viruses reassert and recombine wildly, mixing almost all the known subtypes promiscuously.

There are 18 known hemagglutinin subtypes and 11 known neuraminidase subtypes. Two of each are only known from bats, so there are 16 and 9 that could occur together in birds, for a total of 144 possible combinations.  Some subtypes of each are rare, and some HA and NA types don’t play well together. Which combinations have been found, and how common are each?

Mainly because I was playing with Plotly,1 I tried making a bubble chart of HA and NA subtypes found in waterfowl throughout history.  I used sequences in the influenza databases, sorted by HA and NA, and plotted them with HA on the X axis, NA on the Y, and size of each bubble representing how common they are.

Of course, this is not really a representative look.  It’s wildly distorted by surveillance trends; people intensely test birds for H5N1 (because it’s lethal to humans), and H7N7 was surveyed mainly after multiple people were infected in the 2003 outbreak in the Netherlands, so those are probably over-represented compared to their actual prevalence in birds.  Still, it helps give a sense of the complexity of the viruses circulating out there.

Flu in birds

 


  1. My conclusion: Plotly is pretty cool, but doesn’t offer me very much.[]
February 10th, 2014

How we died in 1890

From the Report on Vital and Social Statistics of the United States at the Eleventh Census: 1890

Malaria 1890
Malaria was a major killer.
Measles 1890
As was measles.
August 26th, 2013

The pace of new virus discovery

From: Search strategy has influenced the discovery rate of human viruses (Proc Natl Acad Sci U S A. 2013 Aug 20;110(34):13961-4)

Virus Discovery
 (A) The cumulative discoveries of human-pathogenic viruses in any organism (black) and their incrimination as a cause of human disease (green). (B) The cumulative discoveries of human-pathogenic arboviruses (red), and nonarboviruses (blue). (C) Yearly arboviruses and nonarboviruses discovered (red and blue points, respectively).

For arthropod-borne viruses, which comprised 39% of pathogenic viruses, the discovery rate peaked at three per year during 1960–1969, but subsequently fell nearly to zero by 1980; however, the rate of discovery of nonarboviruses remained stable at about two per year from 1950 through 2010. The period of highest arbovirus discovery coincided with a comprehensive program supported by The Rockefeller Foundation of isolating viruses from humans, animals, and arthropod vectors at field stations in Latin America, Africa, and India. The productivity of this strategy illustrates the importance of location, approach, long-term commitment, and sponsorship in the discovery of emerging pathogens.

June 24th, 2013

Neutrophil swarm

Neutrophils (red) and monocytes (green) entering an area of tissue damage.

This representative video shows the immediate response of fast-migrating neutrophils (small red cells) towards a focal tissue damage site, while monocytes (green) migrate with slower speeds and follow the developing neutrophil cluster with delay.

–Neutrophil swarms require LTB4 and integrins at sites of cell death in vivo
Tim Lämmermann et al
Nature 498, 371–375 doi:10.1038/nature12175

(See also When Neutrophils Attack)

May 13th, 2013

Deaths in 1898

“Number of deaths per 1000 deaths from known causes” — US Census Office, 1898

(Click for a larger version.)

Top tow, from left: Consumption (scale goes up to “135 and over per 1000 deaths”), diphteria (50 and over), cancer and tumors (30+), whooping cough (14+);

Middle row: Pneumonia (105+), croup (20+), malarial fever (80+), scarlet fever (11+);

Bottom row: Diarrheal diseases (100+), typhoid fever (50+), measles (20+), heart disease and dropsy (80+).

From davidrumsey.com.   

March 25th, 2013

On the Influenza Epidemic of 1892 in London

Table I
London.  Weekly Deaths from “Influenza” during Four Epidemics – 1847-48, 1890, 1891, 1891-92
Table V
London.  Causes of the Mortality due to the Influenza Epidemic of 1892

The link between influenza, and deaths from apparently-unrelated causes, has apparently been noted for well over 100 years. It’s still somewhat controversial today.

Effect on the Mortality from other Diseases.
One of the chief characteristics of an influenza epidemic is the effect it produces on the mortality from other diseases. The disorders most conspicuously affected are, as is well known, those of the respiratory system; but others are influenced in an almost equally marked degree. The annexed table gives details of the relation between the mortality due to various causes of death and that attributed primarily to influenza during the course of the 1892 epidemic.

The principal facts are contained in Table III. Besides the rise in the mortality from the respiratory diseases, the augmented fatality of phthisis, diseases of the circulatory system, and whooping-cough is noticeable, as is also the increase in the number of deaths attributed simply to “old age.”

Another diagram (No. 1) exhibits the dependence of the mortality ascribed to the two main respiratory diseases, bronchitis and pneumonia, on the presence of influenza for the whole period from October, 1889, to July, 1892. It will be seen that in every instance of the prevalence of the latter, the curves representing the mortality from, the two former rise far above the average; The peculiar significance of these curves lies in the fact that the presence of influenza as the primary cause of death was not recognised in any of the cases which they represent; otherwise they would have appeared in the Registrar-General’s returns under the head of “influenza,” and not under that of “bronchitis ” or “pneumonia ” as the case may be.

An increased mortality from all or most of the causes that have been mentioned characterises all influenza epidemics, and not that of 1892 alone. It is impossible to believe that the invariable coincidence between the rise of these various causes of death and influenza is accidental, and the conclusion seems inevitable that influenza itself is the determining cause, though it does not so appear in the returns furnished to the Registrar-General. This being the case, in estimating the mortality of any particular epidemic it is necessary to allow for the deaths returned under other heads than that of influenza.

–On the Influenza Epidemic of 1892 in London :: BMJ 2:353-356 (1892)

February 11th, 2013

Useful information about spider legs

(This post is adapted from two questions I answered on Quora.)

Why do a spider’s legs curl up when it dies?

The explanation was provided by Pritesh Kalantri: Spider legs extend due to hydraulic pressure, not muscular action, so when the hydraulics are turned off (as when the spider dies) the muscles that contract the legs have no opposing action, and the legs curl up.

This was new to me, and I quickly found what seems to be the original paper establishing this fascinating fact:  Parry, D. A., R. H. J. Brown: The hydraulic mechanism of the spider leg. J. Exp. Biol. 36 (1959a) 423–433.

A helpful diagram should you decide to test hydraulic pressure in your own spider’s legs. This can be used with live spiders, as needed.
A more detailed view of spider anatomy

1. The blood pressure inside the leg of the house spider Tegenaria atrica has been measured. Maintained pressures of about 5 cm. Hg and transient pressures of up to 40 cm. Hg have been found.
2. The relation between the blood pressure in the leg and the extension torque at the hinge joints has been established.
3. Considerable torques can be developed at the hinge joints during extension, for example, when accelerating a mass fixed to the leg. The transient pressures found to arise in the leg are adequate to account for these torques.
4. The hydraulic mechanism is discussed. The available evidence suggests that the pressure found in the legs occurs also in the prosoma but not in the abdomen, in which case the maintained pressure must be due to the heart. This, however, requires further investigation.

We are greatly indebted to the Cambridge Instrument Company for the loan of a photo-electric transducer; and also to many friends who have supplied us with spiders.

However, a little further research suggests that hydraulic activity is not the only mechanism for spider leg movement.

In large spiders such as A. concolor, the advantage of strong leg flexion remains valid. Here, during jumps and starts, the net propulsive power is shifted more to their front legs. In contrast to jumping spiders, the ground reaction forces of the frontal legs and the second legs are as strong as those exerted by the hind legs.  … It seems that depending on the spider’s body size both hydraulics and muscular leg flexion contribute, to variable degrees, to the propulsion of the hind legs.

Hydraulic leg extension is not necessarily the main drive in large spiders.
J Exp Biol. 2012 Feb 15;215(Pt 4):578-83. doi: 10.1242/jeb.054585.
Weihmann T, Günther M, Blickhan R.

This led inevitably to the next question:  If you accidentally sever a spider’s leg, will the leg bleed?

It does bleed, but there is a special mechanism that prevents too much loss of fluid.  Here is an explanation from a 1957 paper:

Figure 3.  Anatomy of a spider leg, showing the mechanism by which fluid loss is minimized if the leg is severed

Unlike Crustacea and insects, spiders autotomize their legs at a functional
joint and an account is given of the interesting mechanism by which the joint is severed and bleeding restricted. …

THE AUTOTOMY MECHANISM
‘Autotomie’ was defined by Fredericq (1883) as ‘mutilation par voie reflexe comme moyen de defense chez les animaux’. Usage has since widened the term to embrace all cases of fracture of limbs and other structures at a specific point where structural adaptations associated with the fracture mechanism and reduction of bleeding are found to occur.

… I have shown above (see fig. 3, A-D) that in Tegenaria the coxal muscles are all inserted on to a ring of sclerites which fit into a groove in the proximal rim of the trochanter. The joint fractures between these sclerites and the trochanter, and the coxal muscles then pull the articular membrane proximally while at the same time the sclerites converge on one another (fig. 3, E) so that a comparatively small hole is left in which the blood rapidly clots and which after a day or two is sealed by a brown plate.

— Spider Leg-muscles and the Autotomy Mechanism
D. A. PARRY
Quarterly Journal of Microscopical Science, Vol. 98, part 3, pp. 331-340, Sept. 1957.