Monthly Archives: September 2015

Calico Cats and X inactivation – Embryogenesis Explained Book Excerpt

It has long been a source of frustration to cat breeders that you can’t get the lovely tricolour cat pattern also known as the calico cat, to breed true. Here’s why.1024px-Calico_and_dilute_calico_cats

Two female cats (sisters) illustrating the difference between the calico and dilute calico coats. by Leonardo Boiko

Female mammals have two X chromosomes. (There are a few individual and species exceptions, as always.) Two X chromosomes is one too many and so one has to be shut down in order (presumably) to keep gene dosage at the same level as that in the male. Very early in embryogenesis, when a female mammalian embryo is a small ball of cells, one X chromosome is inactivated in each cell. This inactivated X moves to the outer edge of the nucleus and sits there visible in the light microscope as a Barr body. (Named for Murray Barr who first discovered it.) The timing varies between species so when cats have X inactivation is different in development from when humans have it. Which of the two X chromosomes was silenced in a particular embryonic cell is generally random. Once silenced, that inactivated X is carried on during all future mitoses. There is a gene for coat pigmentation in cats that is also located on the X chromosome. Since females have two X chromosomes they also have two genes for pigmentation. In the female cat, one gene for coat color is shut off when the X is inactivated. If a female cat happens to get an orange gene from one parent and a black gene from the other (she is a heterozygote, i.e. the alleles are different), then during early embryogenesis, the cat will have some cells with only a working orange pigment gene and others cells will have only the black gene working. Both genes, one from the mother and one from the father, are present. Only one is used in each cell because the other is coiled up and sequestered on the inactive X.

The gene for coat pigmentation doesn’t actually “work” until much later in development. Recall the neural crest cells that break free from the boundary zone of the neural ectoderm and the epithelial ectoderm during neural tube closure (Chapter 2). These neural crest cells migrate out and later on some of them form the pigment cells that give us the color we see on the cat. When it is time for the genes to be turned on about half of the calico cat’s cells have only the orange gene turned on and half have the black gene turned on. The pigment cells migrate to their place and then do several rounds of replication to produce patches that are all clones of the first cell to migrate into an area. These patches of cells replicate and expand until they meet cells from another clone. The cat continues developing and the result is the orange and black blotch pattern we see on her coat.

A mutation on a totally separate gene from another chromosome causes the white patches on the calico cat. When this altered gene is active, pigment cell migration is slowed and the cells don’t migrate all the way out to all edges of the cat. They also mix up less than they otherwise would for reasons not really understood. Hence, the white pattern, not associated with the genes on X chromosome, is usually pretty symmetrical on both sides causing the attractive “dipped in milk” look of the classic calico cat. The patches of black and orange are random but larger than on a cat without the white. If the cat has no mutation on the gene, the pigment cell migration is not slowed and she develops into a plainer tortoiseshell cat usually (though not always) with smaller and more blended patches of colour. (Another common allele is an allele called dilute, which makes the colour softer, black to grey and orange to apricot as in the picture.)

The calico cat has one X chromosome inactivated in each cell and the inactivation of that one X is for her entire life. The inactivated state of this X chromosome is transmitted to all copies of that chromosome during subsequent cell divisions and their mitoses. All mechanisms, including DNA methylation, histone modifications and coating by various RNAs such as Xist, that are involved in the transmission of the state of a gene from a cell to its daughter cell at mitosis, are transmitted by bookmarking (Chapter 3). Bookmarking is transmission of a cell’s “memory” to its progeny.

Yet, when a calico cat has kittens she can pass on either the orange gene or the black gene to each of her babies and her kittens will not have the same pattern of inactivation. The male kittens she has will each get one X chromosome from her and one Y chromosome from their father. Because the pigment gene is only on the X chromosome any male kittens will be either orange or black and he will inherit only one of his mother’s coat color genes. What color her female kittens are depends on the both parents’ contribution. If the father is black, he will always contribute one X chromosome with the black gene. The mother can contribute either a black or orange gene. The female kittens will be either black and orange like her or all black, depending on which X they got from their mother. If the father is orange, the reverse happens and the female kittens will be orange or orange and black. The all orange and all black female kittens will undergo their own X inactivation in early development and be just as much mosaics as their prettier calico sisters but the X inactivation pattern will be invisible. X inactivation is “reset” with each generation.

X inactivation was originally discovered by a female scientist Mary Frances Lyon FRS (15 May 1925 – 25 December 2014). Another term for X inactivation is Lyonization.

This post contains excerpts from Chapter 4 of our upcoming book Embyrogenesis Explained.

CalicoCats

Figure Caption: The calico cat is a female cat ♀ with white underparts. The gene for color is located on the X chromosome (vertical line with circle under a cat). The female cat has two X chromosomes and therefore two color pigment genes (two vertical lines with orange and black circles). When the cat embryo reaches about 64 cells X inactivation of one X in each cell occurs. (Nowack, R. (1993). Curious X-inactivation facts about calico cats. NIH Res. 5, 60-65.)The result as it grows is patches of yellow and patches of black in the kitten. Male cats ♂ have only one X chromosome and one Y chromosome (short, vertical grey line) and so are either all black or all orange. The gene which creates white, pigmentless patches is inherited independently of the color genes and is not located on the X chromosome. When a calico cat has kittens she can have an all black or an all yellow daughter with probability ¼, but not both. Which solid color daughter she has depends on the color gene on the X chromosome contributed by the father (left: black father, right: orange father). This is why people often say all orange female cats are relatively rare and why there are no normal male calico cats.

Genetics of Color Vision

Alan and Noah

Picture by Ann Marquez

One of the great things about being both a geneticist and a grandmother is I get to see how genes get transferred around. That shuffling of genes at meiosis produces some really fascinating results. This week I spent time with my youngest grandchild. He is two. He is in that delightful stage when the whole world is a wonder and a joy. His particular fascination now is colors and flowers. While dropping his big brother off at school, we walked past some flower beds of petunias and the little guy was completely taken with flowers.

“Flower, yellow!” (Except it sounded like lellow)

“Flower, Red!”(Pronounced wed)

We wanted some quality time so since the kid was so taken with flowers we decided to visit the Assiniboine Park’s Old English Garden in Winnipeg. This really is an old fashioned English garden with more varieties and colors of flowers in one spot than I have ever seen anywhere else. My grandson was positively in heaven.

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This picture is from the Assiniboine Park website.

“Flower, blue!”

“Flower, lellow!”

And we saw some giant trumpet shaped pink blossoms.

“Flower, pink, BIG!”

He had a wonderful time. In fact we wore him out. All the extra stimulation of the color varieties in the English Garden meant he fell asleep on the drive home and took a longer nap than usual as his developing brain processed all that input.

Watching the little guy it seemed to me that he was seeing a lot more color in these flowers than I was. He is much more fascinated by color than either his sibling or any of his cousins. From testing, I know that I can’t see shades of red as well as I can see shades of blue. I inherited my father’s X chromosome complete with his gene for red/green colour blindness. Fortunately due to X inactivation I am not red/green color blind. My color vision cells are a blend with some cells having the X chromosome I inherited from my father inactivated and in the rest it is my mother’s X chromosome that is inactivated. The result is that I do have an ability to distinguish reds and greens because of the mosaic pattern in my eye but I do have some near color deficits. Due to random meiotic shuffling, none of my sons inherited the red/green color blindness. My sons see color just fine. My brother, on the other hand, was tested in the military and his color vision far exceeds normal. He has such excellent color vision that after he left the military he actually made his living as a color matcher for a kitchen cabinet making company. Being male, he didn’t get an X chromosome from our father. Instead he got our mother’s X and likely something more.

The evolution of color vision in mammals is not a simple progression. Each vertebrate has up to 5 functional visual photopigment opsin genes that clump into two gene families that can be traced back up to 540 million years ago. Four of these genes are expressed in the cone cells in the retina. The other is expressed in the rod cells, which are generally associated with black and white vision but in low light can also have a role in color vision. Mammals started 200 million years ago with one opsin gene on the X chromosome, which itself originated from our tetrapod ancestors about 300 million years ago. For the past 35 million years the catarrhine primates, which include humans, have had two cone opsin genes side by side on the X chromosome, probably as a result of a gene duplication followed by evolutionary divergence. Another opsin gene is located on chromosome 7. With two X chromosomes, human females have two pairs of genes for color vision on them. Males have only one pair. Color blindness is therefore much more common among human males than among human females, my father and I being an excellent example of this when it comes to red.

One of the opsin genes on the X chromosome is called OPN1LW and it codes for protein pigment used by cone cells that respond to the yellow/orange part of the visible spectrum (longer-wavelengths of light). The other gene on the X chromosome is called OPN1MW and it codes for a protein pigment used to detect light at middle wavelengths (yellow/green light). The gene on chromosome 7 that codes for the third opsin gene type is called OPN1SW and it codes for a protein pigment that is used to see the blue/violet part of the visible spectrum (short-wavelength light) Thus there are three different kinds of cone cells, heavily concentrated in the foveal region of the retina, yet each individual cell expresses only one of the three possible opsins. Somehow, there is regulation that ensures one opsin gene, and only one opsin gene, is expressed. These cells are arranged in a patchy manner, including some large patches of one type or another.

With the combination of the three cone cell types we humans have trichromatic vision. A few people have tetrachromatic vision meaning we have four different types of cones and that gives those individuals even more ability to distinguish color. Males can have tetrachromatic vision only if they have two different variations (alleles) of the gene on chromosome 7. They can express one of the two genes on their single X in each cone cell and the two different alleles they have on chromosome 7. I suspect my brother, with his superior color perception has tetrachromatic vision. Females can have tetrachromatic vision in two ways. They can have two alleles on chromosome 7 and they can also have tetrachromatic vision if they have a mosaic pattern in their retina due to X inactivation. In theory, a rare women could even have hexachromatic vision but there is no evidence of that having ever occurred because we simply don’t test beyond tetrachromacy. It would seem that the X inactivation patches are usually too big for tetrachromacy for except perhaps one woman found in an investigated group of 24 women. Even so, it is well established that on average, women have much better color vision than men.

It’s far too soon to tell for certain but I suspect my color obsessed youngest grandchild also has tetrachromatic vision. If that is true, then his visual apparatus is very finely attuned to see all the wonderful colors in the Old English Garden. He will go through life seeing far more beauty than I ever will. And he will wince more often as the less gifted among us wear what appears to his eye as bizarro and clashing combinations.

My husband has green/brown color deficits. He was fascinated by the idea of prosthetic color vision glasses so he could see the world the way we did. He had an undergraduate student, Andrea Wsiaki, who did an undergraduate thesis on “Design of a computer graphics viewer for colour deficiency correction” in 2000. Others have brought this line of research to practical fruition. You can see one of the results here:

A young man gets color compensating glasses and sees purple for the first time in his life.

This young man’s reaction was very similar to watching my grandson in the English Garden

“That’s purple?!! Oh my God!!!”

(This post is based, in part, on material in the epigenetics chapter of our upcoming book, Embryogenesis Explained.)

Progress Report on Diatom Biofuel Producing Solar Panels

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Consider how we get milk from cows: 1. Grow lots of cows. 2. Grind them up. 3. Extract the milk from the mixture. Or did we find a better way?

The standard approach to algal fuels is to grind up the cells and then extract their oil from the mixture. This takes lots of energy to get energy (the oil). The cost of doing this is part of what makes algal fuels expensive. Instead, perhaps we should think of each algal cell as a little cow.

Diatoms are algae that are particularly good at making lots of oil. Their oil includes many low molecular weight alkanes and related molecules. They naturally create everything from propane to jet fuel, or at least molecules a chemical step or two away from the ones we like to burn. Perhaps we could use selective breeding and/or genetic engineering to get diatoms to maximize production of the type of oil we want. There are about 200,000 species of diatoms to start from.

A diatom biofuel solar panel might look much like an electric solar panel, but it would contain live diatoms in water, with some means of milking them. The oil droplets might rise spontaneously to the top, or be separated by a continuous flow centrifuge run by an included electric solar panel.

The advantages of diatom solar panels are many:

  1. Local, rooftop production of gasoline, perhaps as easy as electric solar panels.
  2. No use of cropland to produce biofuels in competition with food.
  3. Works on buildings or nonarable land.
  4. Solves the energy storage problem: we know how to safely handle gasoline, and can use it any time of night or day. (Solar and wind power require battery or dam storage to use when the sun isn’t shining or when the wind isn’t blowing.)
  5. The energy density of gasoline far exceeds that of batteries: 44.4 MJ/kg versus only 0.17 MJ/kg for lead-acid batteries, i.e., 260 times higher.
  6. We would not have to switch from the mature technology of the gasoline engine to electric or hydrogen run automobiles.
  7. Batteries last only 5 years, while gasoline lasts indefinitely until used.
  8. Gasoline can be used to run automobiles, trucks and tractors, and heat and cool homes.
  9. Gasoline can be used to generate electricity.
  10. Gasoline would be equally available everywhere, including remote communities, at equal cost everywhere.
  11. Diatom biofuel solar panels would have zero carbon footprint.
  12. Oil would no longer be a factor in international relations, altering our whole economic system and toppling dictatorships.

In 2009 Dick proposed that diatoms be grown in solar panels and the oil be extracted without killing the diatoms. The work continues in an international collection of scientists in India (lab of Vandana Vinayak), France (lab of Benoît Schoefs), Georgia and Texas, USA (labs of Kalina M. Manoylov and Ali Beskok, and retired diatomists: Mary Ann Tiffany, Stephen Nagy, Richard Gordon). And it’s interdisciplinary: diatomists, algal physiologists, microscopists, nanofluidics engineers, and a theoretical biologist. Research continues on this idea. Some progress includes ways to get living diatoms to give up their oil without much effort on our part.

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Other methods being tested include centrifugation, direct electric current, and titanium dioxide coating of live diatoms.

One problem is that the conditions in a solar panel could get extreme, especially in terms of high temperatures. Fortunately, diatoms are already extremophiles. Diatoms adapted to live in high temperatures already exist. We are presently culturing diatoms from Hot Lake in the state of Washington, USA, the hottest lake in the world where temperatures reach 55C. We will need to survey in situ oil contents of many hot springs diatoms to select the best.

Many practical aspects of making diatom solar panels will have to be addressed:

  • There is a large literature on the ecology of microcosms, enclosed chambers that receive only light energy, but none specifically on diatoms in microcosms.
  • What other organisms (bacteria, etc.) should we allow to live in diatom biofuel solar panels?
  • Will diatoms in a microcosm recycle the nutrients, including silica, from their dead companions?
  • With removal of oil, what nutrients, if any, will need to be replenished? Some might partition into the oil.
  • Will diatoms continue to produce oil if milked at stationary phase in a microcosm?
  • Can we build microcosms for diatoms that are gas permeable, allowing CO2 in and O2 out, while retaining water?

Dick presented this (via Skype) as his second talk “Progress Report on Diatom Biofuel Producing Solar Panels” at the VI-th Vereshchagin Baikal Conference September 7 – 12, 2015, Irkutsk, Russia. The first talk was on diatom motility. Motile diatoms in diatom biofuel solar panels might be able to seek optimal lighting or temperature conditions, if we designed the panels to allow for this.

References:

(Ultimately) Alone in the Universe, by Richard (Dick) Gordon

Loeb2015

I was trying to convince Abraham (Avi) Loeb to join me as an editor of Habitability of the Universe before Earth (HUBE), a book I’m planning in the new book series Astrobiology: Exploring Life on Earth and Beyond (World Scientific Publishing, London) with series editors Joseph Seckbach (Israel), Pabulo Henrique Rampelotto (Brazil) and me (Canada & USA). Now, as Natalie and I have long observed, organizing scientists is much like herding cats. Avi turned me down, despite saying he is very drawn to the subject, on the basis that he is writing yet another book (Books by Abraham Loeb) and that he is heading some sort of award giving group (Breakthrough Initiatives Project of the Breakthrough Prize Foundation). Then he sent me his latest book, available only in Kindle format, From the First Star to Milkomeda. (He did not ask me to do this review.) Milkomeda refers to the result of collision of our Milky Way Galaxy with the “nearby” Andromeda Galaxy “within a few billion years”. Whew! Imagine trying to absorb and assimilate migrants from another 100 billion planets.

This is a semi-autobiographical account of a fine mature scientist and academic who has reached the peak in his career. By reading this book you can see how his mind works and sense his high personal and academic standards. You can also sense the intense loneliness that comes with reaching such a place. It’s a weird book giving you a view most people never see, the workings of an imaginative, clever, sharp, yet careful mind. He is a theoretician, par excellence, with substantial immunity from the grant system and the committees who decide who gets viewing time on expensive, communal telescopes. As a theoretical biologist I understand this independence. It allows our ideas to pour forth.

Avi thinks big. His latest work is on the earliest formation of water in our universe, and the possibility that life developed way back when. I have long been annoyed with the many books on the origin of life that presume, without discussion, that life began on Earth. This is one of the last anthropocentrisms, the first being that Earth is the center of the universe. I had an opportunity to knock the idea down a bit when Alexei Sharov and I wrote Life Before Earth. He came at the problem from a biological point of view, extrapolating a measure of organism complexity back in time, and I helped spell out the consequences. Avi calculates the first time the universe had places warm and cool enough to support liquid water. Both calculations allow for life for most of the 13.6 billion years our universe has been around, not just the paltry 4.54 billion years since the formation of our solar system.

When you start Milkomeda, you think you are about to be treated to a proper autobiography, farm boy near Tel Aviv rocketing to theoretical astrophysicist. But the book in short order plunges into the kind of language one expects in grant applications, giving only hints of Avi’s personal life. As all of Avi’s work is new to me, his 500 or so papers not having crossed my computer desktop previously, I saw past the “justifications” in the grant style of writing to fascinating ideas, like stars doing sling shots around pairs of black holes to achieve speeds near the speed of light. What a ride! Now I have to know whether life on planets around such flying stars would have any chance of surviving the trip? If so, we’d have a mechanism that could spread life well beyond the confines of galaxies. Close encounters with black holes are tales worth telling. I really enjoyed this.

Avi has reached that point in scientific life where he gives much thought to mentoring. A substantial portion of Milkomeda is devoted to the cultivation of the minds of young astrophysicists, trying to strike a balance between them towing the line and being obnoxiously creative. Here Avi shows he is one of us unherded cats. Did you ever hear of a labor union of scientists? No such thing. I’m still nominally President of CARRF, the Canadian Association for Responsible Research Funding, whose members have long since dispersed or departed Earth. My cofounders rejected my preferred moniker UNFUN, the Union of Unfunded Scientists. But under the CARRF banner, we produced much peer reviewed and other literature on how to improve/replace the peer review system for grants. Avi has rediscovered many of these ideas, our tiltings at windmills, unaware of our published efforts. So many scientists independently come to these conclusions, but ununionized, nothing happens. The shame of it all is that the taxpayer, who foots most of the bill for scientific discovery, gets far less bang for the buck than should be possible. I so completely agree with him but I found the whole topic maddening to read about, again. He gives ten specific examples in astrophysics of scientists suppressing the research of other scientists they thought were wrong. It is a warning for anyone who practices science by consensus. If you are someone who has looked with curiosity at the inner workings of astrophysics and wondered what being in the field is about, this book will give you keen insights.

Good ole Lord Kelvin predicted the Heat Death of the Universe, back before nuclear energy was discovered, a rather depressing scenario. Avi, while holding his head high in contemplating the universe on the cover of Milkomeda, points out that with the universe expanding, most of the galaxies we see beyond our local cluster will vanish from the sky. Their light will not reach us, because the rate of expansion of the universe exceeds the speed of light. Somehow gravity will keep our small corner of the universe intact, but alone. Well, perhaps: another depressing outcome. But maybe we could hitch a ride around that pair of black holes from the Milky Way and Andromeda as they hurl towards each other, and be out of here. Stay tuned. And buy the book. You still have time.

Diatom Motility – Explosive Breakthrough in Understanding

Slide08

There are several models of how diatom motility works:

Snail-like movement (proposed by Christian Gottfried Ehrenberg in 1838)

Jet engine like motion using a form of jet propulsion (proposed by Carl von Nägeli in 1849, modified by C.Th. von Siebold in 1853), long before the jet engine was invented!

Rowing model (proposed by J. Hogg in 1855)

Rocket ship model: O. Bütschli (1892) and Robert Lauterborn (1896) proposed that a sticky jelly-like substance, extruded quickly in fine threads at the nodules of the raphes, propels the cells by mechanical recoil.

Extroproplasm streaming model think of a tank tread (proposed by Otto Müller in 1893)

And then there is capillarity (Flame of Life) model: Slide24

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A new competing model by Lesley Edgar and Jeremy Pickett-Heaps (1983) proposes that the raphe fibers are passively carried by myosin motor molecules.

The problem of diatom motility is still unsolved.

Lesley Ann Edgar (1955-2006) analyzed movie films of motile diatoms at 10 frames per second and noted erratic accelerations to 100 µm/sec2 (see Edgar, L.A. (1979). Diatom locomotion: computer assisted analysis of cine film. Br. Phycol. J. 14, 83-101.)

  • “It is possible that such a strand is secreted in short units corresponding to release of individual loads of locomotor material from within cytoplasmic vesicles through the plasmalemma, so that locomotion would occur in a series of steps” (Edgar, L.A. (1979). Diatom locomotion: computer assisted analysis of cine film. Br. Phycol. J. 14, 83-101.)

Hm….very interesting result. So we (working with Can Sabuncu and Ali Beskok at Southern Methodist University) followed up, and got the same result, even though our camera is nearly 1000 times faster:

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We may be seeing very high speed forward and backwards movement. So maybe the rocket propulsion model is right: strands of mucilage are extruded along the raphe. They hydrate on contact with water exiting the raphe in chemical explosions. These repeated explosions move the diatom along in spurts. The mucilage is left behind as the sticky “diatom trail”. Its elasticity sometimes pulls the diatom backwards as the connection with the trail is stretched and breaks.

Is this correct? We need more research. Our next plan includes computer simulation:Slide36

This blog is a summary version of:

History and future of understanding the mechanism of diatom motility
6TH INTERNATIONAL VERESHCHAGIN
BAIKAL CONFERENCE
AND 4TH BAIKAL SYMPOSIUM ON MICROBIOLOGY (BSM-2015)
MICROORGANISMS AND VIRUSES IN AQUATIC ECOSYSTEMS
September 7-12, 2015

Richard Gordon

Gulf Specimen Aquarium & Marine Laboratory, Panacea, Florida, USA

Ali Beskok & A. Can Sabuncu

Department of Mechanical Engineering

If you would like a copy of the full presentation, please send us a message.

Diatoms are forever.

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Centric Diatom (Mary Ann Tiffany)

On Thursday last week Dick was giving a seminar to a group of Russian scientists in Irkutsk on Lake Baikal via Skype. The people there were all familiar with diatoms so before I report on his presentation, I thought I would give some background on diatoms.

Diatoms are unicellular, eukaryotic, photosynthetic algae that are found in aquatic environments. Diatoms have enormous ecological importance on this planet and display a diversity of patterns and structures at the nano- to millimetre scale.

Diatoms are microscopic (2 µm to 4 mm), and species are classified mostly by the shapes and patterns of their hard silica parts. There are 􏰀250 living diatom genera with more than 200 000 estimated species classified by their unique morphologies. The silica (glass) shell, or ‘frustule’, consists of two overlapping valves joined with silica girdle bands, much like a Petri dish. There are two major groups that are separated based on valve symmetry. The pennate diatoms are elongate, usually with bilateral symmetry. Centric diatoms have radial symmetry. The pennates are placed into two classes depending on whether or not they have slits in the valves called raphes. These slits are involved in gliding motility. Dick has been studying diatom motility for most of his adult life and the above is adapted from his review article “The Glass Menagerie: diatoms for novel applications in nanotechnology”

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Pennate diatom without a raphe (Mary Ann Tiffany)

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Pennate diatom with two raphe slits (Mary Ann Tiffany)

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Close up of a raphe, which goes clear through the shell (Mary Ann Tiffany)

Gardeners are familiar diatomaceous earth which is mostly diatom shells. You are most likely familiar with diatoms for their killer aspect. Diatoms are what gives rocks in running water that lovely slick coating that makes falling in rivers and creeks so easy. During a trip to Yellowstone, we saw a man wading across the rocky bottom of a fast moving small river about 10 meters back from the edge of a five story waterfall. We left before we were forced to to witness the diatoms killing this poor fellow in front of his wife and children. We later reported this to a ranger who sighed deeply and said “Yellowstone is the Olympics of the Darwin Awards. Too bad this guy has already reproduced.”

You can read more about diatoms in a great Wikipedia article. In the meantime here are a couple more of Mary Ann Tiffany’s wonderful images which she has so graciously given us permission to share. Diatoms Are Forever is the title of a book we are working on with a few diatomist colleagues.

Electron Image 41HalfMoonBayht600 Electron Image 52