Wednesday 31 October 2018

Gouldian Finches and Guillemots. H.N. 'Mick' Southern

Sometimes when you are reading up on a subject a surprise awaits. You find that somebody you associate with another field has published in the field you have become interested in. One such recent case was my post on recent research that pinpoints the genetic difference in head colour of the Gouldian Finch. I did not know that the ecologist H.N. ‘Mick’ Southern had worked on that problem but there it was, a paper in the Journal of Genetics in 1945, Polymorphism in Poephila gouldiae Gould. I then learned from his obituaries that he was interested in polymorphism in birds, especially that in the Common Guillemot (Uria aalge) where the ‘bridled’ morph exists alongside the ‘normal’ morph but in increasing frequency the further north in the geographical range of this species.

Henry Neville Southern (1908-1986) was a member of Charles Elton’s Bureau of Animal Population at Oxford. He graduated twice, first in classics, then after a spell in publishing in zoology. As an undergraduate the first time round he had a book published on bird photography. An ecologist who was claimed by the ornithologists as one of their own and by mammalogists as of their tribe he was particularly well known for his long-term studies on wood-mice and on one of their major predators, the Tawny Owl. He edited and wrote a great deal of The Handbook of British Mammals published in 1964 by Blackwells.

Never having moved in ecological or Oxford zoology circles (‘a place best avoided’ was the advice of my PhD supervisor) I did meet ‘Mick’ Southern once. He, John Perry and I were at an old Zoological Club dinner in the 1970s. ‘Mick’ and John were wartime colleagues at the Bureau of Animal Population, when the emphasis was on the control of mammalian (rats, mice, rabbits) and avian (Wood Pigeon, House Sparrow, Rook) pests which were endangering British food supplies and the crews of additional ships needed to bring food by sea through U-boat infested waters.

Photographs of Bridled and 'Ordinary' Common Guillemots

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and the red-headed morph of the Gouldian Finch

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Friday 26 October 2018

The Kimberley, Australia: A Robert Mertens Day

In the early 1960s, the name Robert Mertens (1894-1975) was well-known to anybody in Britain keen on reptiles because the translation of his book, The World of Amphibians and Reptiles*, hit the bookshops and libraries in 1960. The publication of books on reptiles and amphibians was a pretty unusual event and it joined the other popular survey by Schmidt † and Inger. Living Reptiles of the World, published in 1957 but taking a very different approach.

These books though were expensive. Mertens sold for £3-3s-0d. The equivalent price today is £63 if calculated on the increase in retail prices, £136 if calculated on the increase in pay. I had Schmidt and Inger (the same price) but had to make do with Mertens renewed countless times from the local library. As a result I did not have a copy until I bought one for a few pence several years ago.

Mertens, although a museum man through and through, kept a large collection of animals at work and at home. His survey included what was known of behaviour, ecology and physiology rather than just a review of the kinds of living animals and their taxonomy.

Robert Mertens
Contributions to the History of Herpetology
Gradually, I found other work that Mertens had done, for example, on the European lizards and his checklist of European reptiles. I also heard of how he died (see later). However, only when I read the biography in Contributions to the History of Herpetology, did I become fully aware of his work.

In brief, Mertens was born in Russia to German parents—his father was a fur trader. Because of the social unrest that eventually exploded as the Russian Revolution he went to a German university, Leipzig to study medicine and biology. He served a short time in the German army and then joined the Senckenberg Museum in Frankfurt in 1919 where he stayed for the until his retirement in 1960. From 1947, he was Director of the Museum. From 1930 he was also a professor at the University of Frankfurt.

During the Second World War, he spread the collection around Germany and operated a scheme to receive specimens collected by keen soldiers by using the army’s field post system. Imagine the scene on either side of the front line in North Africa as German herpetologists studied and collected the fauna while British and Commonwealth herpetologists, like John Cloudsley-Thompson (1921-2013) of the 7th Armoured Division (Desert Rats), beavered away on the other.

On the Mitchell Plateau in the Kimberley of Western Australia, Mertens is commemorated geographically as well as zoologically. This is because he travelled, collected and explored  extensively in tropical regions including northern Australia and the Indonesian islands. In May, as we walked to Mitchell Falls we passed Little Mertens Falls, waded across the top of Big Mertens Falls and some us saw (I just got the end of the tail) Mertens’s Water Monitor (Varanus mertensi). The newly-described monitor was named in Mertens’s honour by Ludwig Glauert in 1951 (more on Glauert of the Western Australian Museum, Sheffield born and a Sheffield graduate in another post). The naming was highly appropriate—Mertens was the world expert on varanid lizards.

Arrow shows the location of Mertens Falls

Little Mertens Falls
From the cave behind Little Mertens Falls
Big Mertens Falls

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Merten's Water Monitor above Little Mertens Falls

Beyond finding that the two sets of water falls on the Mitchell Plateau were named for him, I have been able to find nothing on when this was done nor by whom it was done. Those who walk or are flown by helicopter over his falls to the Mitchell Falls have no idea who Mertens was or of his role as one of the leading herpetologists of the 20th Century.

There is very little information on Robert Mertens in English and I do not know when he travelled in the northern part of Western Australia. From a list of some of his publications, I would assume the 1920s or 30s. What is known is his sad end. He had kept for a long time a rear-fanged vine or twig snake. When I read about this at the time it was Kirtland’s Vine Snake (Thelotornis kirtlandii) and that identification still appears in some publications including Manson's Tropical Diseases. More recently it is shown as T. capensis from further south in Africa. Whatever the species, it bit him on 5 August 1975. Mertens was 90. No antivenin had been made for this species and eighteen painful days later he died. Throughout that period he kept a diary and ended it with the famous line, ‘a singularly appropriate end for a herpetologist’.

†Karl Patterson Schmidt (1890-1957) of the Field Museum in Chicago, and with similar wide interests to Mertens, died as a result from the bite of another African rear-fanged snake, the Boomslang, Dispholidus typus, in 1957. A single fang of a small specimen caught him and after declining any treatment recorded its effects on him. He died the next day.

*The book first appeared as La Vie des Amphibiens et Reptiles in 1959 with the English, Italian and Spanish editions following. There seems to have been no publication in German. One of the reasons why it was so good is that it was translated into English by Hampton Wildman Parker (1897-1968), retired Keeper of Zoology at the Natural History Museum in London and before that, head of herpetology.

Anon. Mertens, Robert (1894-1975). 2014. In, Contributions to the History of Herpetology, Volume 1, revised and expanded. Edited by Kraig Adler, pp 98-99. (Contributions to Herpetology 30, Society for the Study of Amphibians and Reptiles).

Glauert L 1951. A New Varanus from East Kimberley, Varanus mertensi sp.n. Western Australian Naturalist 3 (1, July 20, 1951), 14-16.

Mertens R. 1960. The World of Amphibians and Reptiles. London: Harrap.

Schmidt KP, Inger RF. 1957. Living Reptiles of the World. London: Hamish Hamilton.

Monday 22 October 2018

Red-heads and Black-heads. New research finds the gene controlling head colour in the Gouldian Finch

The Gouldian Finch (Chloebia or Erythrura gouldiae) is famous for a number of reasons. The first is a sad one. It has become rare in its habitat of tropical northern Australia because of agricultural practice (burning grassland at the wrong time of year and the introduction of domestic livestock in areas which reason indicates should actually be left wild). The second is that it occurs in three colour morphs in the wild. The third is that because of its beauty it has always been a popular bird with aviculturists in Europe, North America and Japan.

The third reason (i.e. its popularity in aviculture) is responsible for the generation of so much knowledge about this species which has been put to good use in devising conservation measures  in the wild by halting, apparently, the precipitous decline in the size of the population and, even though only a few thousand birds of this small seed-eating bird remain, the possibly unwise lifting of its status from ‘Endangered’ to ‘Nearly Threatened’.

The breeding and maintenance of stocks of the Gouldian Finch in aviaries has also facilitated the recent discovery of the genetic mechanism responsible for the difference in head coloration of the morphs. For this article I am going to ignore the orange-headed morph which occurs at very low frequency (less than one in a thousand individuals). In the wild, the ratio of black-headed to red-headed individuals is 7:3.

From Toomey et al. 2018

Thanks to breeding records in captivity, it has been known for many years that the genetics of head colour can be explained by simple sex-linked Mendelian inheritance with the allele for red being dominant and black recessive. In 2016 this Red gene was located on the Z chromosome. In birds, the sex determination is not the same as in mammals. Male birds have two Z chromosomes, females one Z and one W.

Before going on to describe the very recent genomic work, I should point out that there are differences, discovered, again, by research on birds in captivity between the two colour morphs, in addition to the differences in head colour. Red heads are more aggressive and dominate in encounters with black heads. In competitive social environments, red heads show increased concentrations of testosterone and corticosterone in their blood whereas black heads do not. There is also assortative mating, red heads prefer red heads, blacks black. Clearly, whatever the genetic mechanism it is pleiotropic, i.e. affects a number of traits within the body.

A group of authors from U.S.A. and Portugal have now tracked down the locus of Red gene to a small region on the Z chromosome. The gene itself is on part of the chromosome that does not encode a protein that can be responsible for its actions in the body. However, it is in a position to control a nearby gene that encodes for the protein, Follistatin, and indeed the group provides evidence that it is the production of Follistatin which controls head colour as well as the other physiological traits. There is also evidence that Follistatin could be involved in controlling the differences in plumage colour between other species of bird.

There is still much work to be done on the ‘how’ or mechanistic questions as well as the ‘why’ questions such as why, given the stroppiness and dominance of the red-head over the black, the overall ratio of 3:7 has remained unchanged.

Finally, since you ask, have I ever seen in Gouldian Finch in the wild? No. Even though I have been to northern Australia several times and passed through their known range, I have not had the chance to go to one of the known hot-spots of the remaining population.

Toomey MB, Marques CI, Andrade P, Araújo PM, Sabatino S, Gazda MA, Afonso S, Lopes RJ, Corbo JC, Carneiro M. 2018 A non-coding region near Follistatin controls head colour polymorphism in the Gouldian finch. Proceedings of the Royal Society B 285, 20181788.

Legge S, Garnett S, Maute K, Heathcote J, Murphy S, Woinarski JCZ, Astheimer L. 2015. A landscape-scale, applied fire management experiment promotes recovery of a population of the threatened Gouldian Finch, Erythrura gouldiae, in Australia’s Tropical Savannas. PLoS ONE 10(10): e0137997. doi:10.1371/journal.pone.0137997

Classic Reads:

Mike Fidler (who has made enormous financial and practical contributions to the conservation and study of the Gouldian Finch in Australia an UK) and Stewart Evans (1936-2010) late of the University of Newcastle, UK. The Gouldian Finch. 1986. Blandford Press.

Derek Goodwin (1920-2008). 1982. Estrildid Finches of the World. London: British Museum (Natural History) and Oxford University Press.

Gouldian Finches have been kept and bred since the 1870s. This drawing
illustrates an article on cage-bird traffic of the U.S.A. by Henry Oldys
published in the Yearbook of the U.S. Department of Agriculture 1906

Monday 15 October 2018

Joan Procter and Chalmers Mitchell: ‘Vita’ Glass at London Zoo in the 1920s

If you stand close to the small vivaria lining the western outer wall of London Zoo’s Reptile House and look upwards you will see daylight. Natural light was admitted as part of the design not because of any wish to save electricity but for the good of the inhabitants. The glass in the roof of the house and the vivaria was not ordinary glass but Vita, a glass of special composition to allow the transmission of rays at the ultraviolet end of the spectrum.

Entrance to the Reptile House, 2011
Photograph by William Hook via Wikimedia

Joan Procter’s inclusion of Vita glass was just one manifestation of the Zoo’s pioneering efforts, through Sir Peter Chalmers Mitchell FRS, to improve the health of zoo animals. In fact, he was riding the crest of a scientific and populist wave sweeping across the world in the inter-war years that can be summed up as: fresh air, sunshine and vitamins. The architect, John Stanislav Sadar has put the whole development of Vita glass in that context. In short, because ultraviolet rays were known to kill bacteria, and their importance in the synthesis of vitamin D was emerging, sunlight must be good for you. Put into the context of the industrial urban environment: poor housing; enormously high levels of air pollution, and the consequent human diseases of rickets, tuberculosis and chronic respiratory morbidity, it is hardly surprising that scientific, clinical,  social and commercial efforts combined to promote the outdoor life, sunshine and patent medicines.

In the 1920s it was known that ordinary glass blocked the transmission of ultraviolet rays in sunlight. Ergo, glass that would transmit ultraviolet would be healthier. To solve this problem, Francis Edward Everard Lamplough (1881-1975) appeared on the scene.

Whether Lamplough thought of the idea himself or was urged to try by scientists or others in the sunshine movement is not clear. This is what he had to say in his lecture to the Royal Society of Arts in 1929:

The scientific research involved was carried out with much encouragement from Professor Leonard Hill, and also from the authorities of the London Zoological Gardens, Dr Saleeby [Caleb Williams Saleeby, 1878-1940] and others, and early in 1925 the first full scale melting was made of window glass (designated “Vita”) pervious to the health rays.

Professor (later Sir) Leonard Erskine Hill FRS (1866-1952) was the scientific leader of the fresh air and sunshine movement. He was Director of Applied Physiology at the National Institute of Medical Research. Hill’s main interest was in using lamps that emitted in the ultraviolet or infrared to mimic the effect of sunlight on the body for therapy and prevention of rickets, for example. The Times (22 May 1928) carried the story of how Hill came to be involved:

Early in 1925 the Council of the Zoological Society of London had under consideration the construction of a new Monkey House. The existing house, built in 1864, provided no open-air cages and was arranged on the theory that artificial heat was the primary requirement for the health of these animals. Dr. Chalmers Mitchell, Secretary of the Society, had shown in 1911 by an elaborate study of the mortality statistics in the Zoo for a period of over 30 years, that health was better and the duration of life longer in monkeys (and most other warm-blooded creatures) kept with free access to the open air in all weathers and without artificial heat. Later observations showed that, although cold air was better than warm, stale air, good hygiene required also radiant heat and sunlight.
     It was decided before going to the expense of constructing a large new Monkey House to erect a small-scale experimental house in which the theoretically best conditions might be tried out during at least one winter. Fresh air and heat were easy to provide, and Dr. Leonard Hill, F.R.S., who had been working out proper, conditions for sickly children at the National Institute of Medical Research, Mount Vernon, Hampstead, and who had studied the conditions in the houses in the Gardens, described to Dr. Chalmers Mitchell the part played by ultra-violet rays. He advised the provision of electric light in globes of fused quartz which was almost, completely transparent to the health-giving rays. He also, informed him of certain laboratory experiments with a new form of glass, called “Vita” glass, which had not then been made on a commercial scale, but which was transparent to the ultra-violet rays of sunlight which were cut off by ordinary window glass. Dr. Mitchell, on behalf of the Zoological Society, commissioned the inventor of “Vita” glass to make a sufficient quantity to glaze the experimental house.
     The usual difficulties in the change from laboratory to manufacturing scale arose, but were surmounted, and the Zoo's experimental house was the first building to be provided with “Vita" glass. Spectroscopic examination showed the transparence of the new material to ultra-violet rays, and the effect on the animals was so good that the Lion House and the new Reptile House, and, later, the full-size new Monkey House, were all lighted with “Vita” glass with complete success in every case, as shown by the better health and better spirits of the animals.
Sir Leonard Erskine Hill (1866-1952) in 1934
Bassano Ltd. National Portrait Gallery

I have been able to find surprisingly little about Lamplough. Educated at Oundle and Cambridge he was awarded a First in Natural Sciences in 1904. Elected a Fellow of Trinity College in 1906, he also served as Additional Demonstrator in Chemistry between 1914 and 1917. He married Augusta Gertrude Stewart in 1907. At the start of the Second World War, he was working at the Royal Aircraft Establishment, Farnborough. He died in 1975 at Woodchester, Stroud, Gloucestershire. During the work on Vita glass he is described as Late Fellow of Trinity College, Cambridge. My impression is that he was working for Chance Brothers, the famous makers of glass and lighthouses (he had patents for a gas valve used in lighthouses in 1920-21), throughout this period though perhaps not as an employee but as an independent inventor or consultant. He was also the inventor (The Times 22 May 1928) of the artificial daylight ‘Daylamp’ and a glare filter for Chance.

Lamplough’s development of a low iron content glass that transmits in the ultraviolet range depended on the findings of Sir William Crookes that oxidised ferric iron absorbs, whereas ferrous iron transmits, ultraviolet. The Chance works would have been highly familiar with Crookes’s work since they were responsible for developing and manufacturing special ultraviolet-blocking glass. 

Spectrographs showing the transmission through Vita compared with
ordinary window glass. From Lamplough's RSA paper

The Times 22 May 1928

After the installation of Vita glass at the Zoo, the New Health Society (i.e. Hill et al.) and Saleeby’s Sunlight League promoted its use in hospitals, schools, farms and greenhouses. The Times (25 April 1933) reported that Vita glass had been installed at Clifton College in Bristol and (3rd October 1929) on a veranda roof at a hospital.

Advertisements in The Times in 1928 and 1932

When Marlborough House was being prepared for occupation by the then Prince of Wales The Times (8 November 1927) reported that his ‘business room’ was glazed with Vita. Perhaps that’s why he had the energy to pursue Mrs Simpson. Domestic houses were also targeted for sales. Indeed, those involved saw it capturing the entire market for window glass. But that optimism was not justified. Production ceased in the 1930s and stocks were gradually sold off. What went wrong?

The reasons for the rapid decline in sales of Vita glass are a mixture of doubts over efficacy, errors made in the commercial arrangements for manufacturing and marketing, price and competition. Although Lamplough dealt with the technical problems in his lecture in 1929, namely, the early, rapid but partial loss of transmission of ultraviolet when Vita glass was exposed to sunlight and the problems of dirt and grime settling on the glass, doubts remained, apparently, on its efficacy under natural conditions on buildings.

The manufacture and marketing arrangements, described by Sadar, must be an object lesson in how not to do it for business students. Chance Brothers sub-licensed* Vita plate-glass manufacture to Pilkingtons; marketing for both companies was done jointly by the ‘Vita’ Glass Marketing Board which not only caused problems for the marketing departments of the two companies but also inadvertently advanced the cause of rival and better products appearing on the world market. Tests in the U.S.A. showed that Corning’s Corex glass allowed much greater transmission of ultraviolet than Vita. I do not know if Lamplough, or the two British glass manufacturers, tried to improve his glass as better glasses appeared. Finally, there was the price which Sadar estimates as six times more expensive than ordinary window glass. In the relatively affluent 1920s installing Vita might have been seen as ‘the’ thing to have by the worried unwell (like the silly ‘health’ foods of the 2010s) or public bodies trying to improve the health of schoolchildren but by the economically depressed 1930s specifying or choosing an expensive window glass would have been a different matter. A few minutes’ exposure to natural sunlight was of course more effective in synthesising vitamin D  than hours spent behind a Vita glass window.

All the promotion of the health-promoting properties of ultraviolet ignored the growing evidence of the dangers of excessive exposure of the skin and eyes, much of it provided by Hill!. But by the 1930s such actual or possible deleterious effects of the more extreme examples of therapy by sunlight were being recognised and the medical craze of the 1920s began to fade away, to be replaced by vitamin supplementation and the careful use of high-intensity sunray lamps. In most domestic and public spaces we can only be thankful that ordinary window glass is impermeable to the ultraviolet end of the spectrum unless, of course, we fancy a getting a suntan behind the privacy of our french windows.

Two questions remain on Joan Procter’s Reptile House. The first is whether or not sufficient ultraviolet rays reached the inhabitants for the synthesis of Vitamin D. Looking at the technological solutions now applied to vivaria to supply sufficient ultraviolet to many reptiles in captivity I doubt it. The second is whether any of the Vita glass on and in the Reptile House has survived (the less than successful Monkey House was fortunately demolished in 1970 as was the Lion House). If it has, then there is a solution to the first question since the natural ultraviolet irradiance in the vivaria can be measured. However, also installed in the Reptile House were some of Hill’s ultraviolet and infrared lamps. Vita glass was also used in a very different role to that in the windows—as a cover the quartz (ultraviolet emitting lamps) lamps to shield out the short wavelengths which had proved fatal to lizards.

Original layout of the Reptile House. Only at the two ends of the building have there been changes
in inhabitants. The Times 15 June 1927

Successful in the Reptile House or not, the installation of Vita glass shows the determination of Chalmers Mitchell and Joan Procter to make London Zoo part of the movement to improve living conditions for all inhabitants of industrial Britain in the early decades of the 20th Century and to bring scientific advances to bear on problems of wild animal husbandry. As far as the Zoological Society is concerned the culmination of the fresh air and sunlight school was the opening of Whipsnade Zoo in Bedfordshire on 23 May 1931, four months before Joan Procter’s death.

*I have been unable to find any patent by Lamplough on Vita glass. Chance probably relied on protection by know-how rather than releasing the formula in a patent.

†Those aware of Chalmers Mitchell’s other jobs will realise that the reports ON him for The Times were probably written BY him as science correspondent for that newspaper.

Sadar JS. 2012. ‘Vita’ glass and the discourse of modern culture. In, Writing Design, edited by G Lees-Maffei, pp103-117. London: Berg.

Lamplough FE [he often omitted the second E). 1929. The properties and applications of “Vita” glass. Journal of the Royal Society of Arts 77, 799-811.

Tuesday 9 October 2018

Joan Procter and Sir Peter Chalmers Mitchell. Scandalous Rumours at London Zoo and Whipsnade in the 1920s

I was looking for information on somebody else entirely when I came across the passenger list of SS Highland Rover’s voyage from London to Argentina in 1925. The names that caught my eye on board this ship, which carried Argentinian beef as well as passengers on the return voyage, were Peter Mitchell, aged 60, and Joan Procter, aged 28, both giving their address as Zoological Society of London and their occupation as ‘Zoologist’. Peter Mitchell was better known as Sir Peter Chalmers Mitchell FRS (he was knighted in 1929), Secretary of the Society, or Chief Executive in modern terminology; he used the Scottish non-hyphenated form of double-barrelled surname, Chalmers Mitchell, even though, legally, his surname was Mitchell; Chalmers was his mother’s maiden name.

SS Highland Rover

Joan Procter’s story is very well-known*. In 1925 she was Curator of Reptiles at the Zoo. Illness had prevented her from taking up a Cambridge place, her all-consuming interest in reptiles led to her first assisting George Albert Boulenger FRS at the Natural History Museum then being given a paid place. She became an expert in herpetology and in display techniques. She was recruited to the Zoo by Chalmers Mitchell to take over the reptile collection from Edward George Boulenger, son of G.A., who moved to be Curator of the newly constructed aquarium. She designed the new reptile house, became an expert at all aspects of reptilian husbandry and was instrumental with Mitchell in pulling the Zoo into the 20th Century. She did all this while crippled with pain and while often confined to an electric bath chair.

Rumours that Mitchell, who was at least distant and perhaps estranged from his wife for a time, and Procter were lovers were rife in the 1920s and 1930s; indeed they persisted at least until the 1990s whenever his name came up in conversation with people to whom the story had been passed down the line from the 1920s. But were the rumours based on fact? In his entry on Mitchell for the Oxford Dictionary of National Biography, John Edwards wrote:

During the 1920s Chalmers Mitchell developed a close friendship with Joan Beauchamp Procter (1897–1931), curator of reptiles at London Zoo. Despite the distant relationship with his wife, and contemporary gossip, there is no evidence that she was his mistress—her poor health would probably have prevented the relationship from being other than platonic.

Well, perhaps, but there is no doubt that some events set tongues wagging. It is easy to imagine people putting two and two together and getting five—or four—during their weekend or her recuperative stays at Whipsnade when it was being transformed from farmland into a Zoo.

I can only imagine the rumour mill grinding with the news that the two were travelling together to Las Palmas, clearly for the Christmas period of 1925 (the ship sailed on 17 December) when Miss Procter had only been at the Zoo for two years. But in this did they-didn’t they story it is worth pointing out that Joan Procter travelled with a nurse, an Ann Carter, aged 35, a situation hardly conducive to goings-on of an amorous nature.

But given the parlous state of Miss Procter’s health I do find it surprising that between 1925 and her death in 1931 she made other voyages. I found three: SS Tanganyika (Hamburg America Line) to Malaga which left Southampton on 6 January 1928; P&O’s SS Rajputana to Marseille which departed on 12 August 1929; P&O’s SS Cathay, also to Marseille which departed on 7 July 1931. She must have returned to London from the latter trip only weeks before she died on 20 September 1931 at the age of 34. The significance for the present discussion of the trip to Malaga is that Mitchell had a house (Villa Santa Lucía) there which he first rented so that Joan Procter could convalesce after being taken very ill while on holiday in 1927.

It may—or may not—be significant that by 1935 Michell was travelling, to Gibraltar in the case recorded, with his wife again, although the wife is not mentioned in his book of the period, My House in Málaga (Faber & Faber, 1938).

There is a correction to some of the accounts of Joan Procter’s life—and death. In some it is stated that she died from cancer. However, it seemed to me that her illness(es) were too prolonged for that to be the case. At a dinner one night I spoke to two elderly London physicians who were familiar with the medical practitioners and practices of the inter-war years in London. They agreed. I then found her ODNB entry written by Howard Bailes, a teacher at St Paul’s Girl School where she was educated: chronic intestinal illness was how he described the condition that prevented her from going to Cambridge. Given that information I ordered a copy of her death certificate. The cause of death was: I(a) (i.e immediate condition) Heart failure, I(b) (i.e. due to condition) Toxic myocarditis, I(c) (i.e. other condition) Pyelo-cystitis. B. coli, II (i.e. contributing condition) Old pyloric ulcer, peritoneal adhesions, colitis. No P.M. (post mortem, autopsy).

There is no mention of the previous operations outlined in an obituary in The Times, probably written by Mitchell, that could have caused the adhesions and so much pain. It is perhaps not surprising in her condition, weakened by colitis, the ‘old’ ulcer and adhesions, that she fell victim to an infection (B. coli is now, of course, Escherichia coli) of the renal tract which according to the medical literature of the time may have been of long-standing, even congenital, which spread to the heart. We need no reminding that these were pre-antibiotic days.

Joan Procter is rightly remembered for her achievements—judged utterly remarkable for a woman at the time, especially by the news media who still seemed unwilling to believe women could do or would want to anything properly, let alone handle snakes or Komodo Dragons. Her marble bust sits high on the wall of her creation, the Reptile House at London Zoo—built to her precise design with the architect only adding the fancy bits on the outside. An appropriate addition to the memorial would be from Sir Christopher Wren’s epitaph on his tomb in St Paul’s Cathedral: Si monumentum requiris circumspice.

An iPhone shot of the memorial to Joan
Procter in the Reptile House at London Zoo

Sadly, few people notice her memorial and I do wonder what she would make of the uninterested feral parties of London schoolchildren rampaging through the Reptile House who with their completely incompetent teachers have ruined my now-rare last two visits there.

As to what was the relationship between Miss Procter and her boss (who he described as 'dear friend, ward and colleague'), was it a typical case of there must-be-something-in-it type of vicious rumour propagated by their staff? Or was Joan Procter treated as a daughter that Mitchell never had? Or...?

*The most complete biography is in Volume 2 of the series Contributions to the History of Herpetology, edited by Kraig Adler, Society for the Study of Amphibians and Reptiles. 2007. Also see  Bailes H. 2004 .Procter, Joan Beauchamp (1897–1931), herpetologist. Oxford Dictionary of National Biography. Edwards JC. 2004. Mitchell, Sir Peter Chalmers (1864–1945), zoologist. Oxford Dictionary of National Biography. Obituary: Miss Joan Procter. The Times, 21 September 1931.

Modified 6 May 2021

Wednesday 3 October 2018

Mabel Hokin and Salt Glands: My sad demolition of a biochemical treasure

Having worked on bird salt glands in Hong Kong I arrived at Babraham in October 1968 to work on the mammary gland and the mechanism of milk secretion—a very different gland and a very different fluid being produced.

During that summer Jim Linzell had attended a satellite symposium of the Washington Physiological Congress on exocrine glands and had heard Mabel Hokin give a talk on the bird salt gland. He told me about this and since a similar approach might provide information on the mechanism of secretion of the aqueous phase of milk, I set about doing similar studies on the mammary gland. However, when I read Mabel Hokin’s work in greater detail I realised there were some anomalies. I will not go into great detail but the concentrations of sodium, potassium and chloride ions in salt-gland slices appeared to be much higher than those reported by others. This mattered since by calculating the concentrations inside the cells from a knowledge of the size and composition of the extracellular space, she concluded that the high concentration difference of sodium chloride was established between blood and the inside of the cell, not between the cell and the lumen of the gland, as previous evidence had suggested. I, egged on by Jim Linzell and Richard Keynes FRS who was then Director of the institute and gathering information for his masterly review of ion transport mechanisms across membranes in different organs, thought it wise to repeat the Hokin experiments.

I was unable to get the same results as Mabel Hokin. The concentrations inside the cell appeared similar to other non-nervous tissues, implying that the high concentration gradient for salt is set up between the cell and the lumen of the gland, the later leading to the duct system and the flow of salt-rich fluid to the outside world.

The difference between mine and her results rested on the crude concentrations of sodium, potassium and chloride in the tissue, before any calculation of concentrations inside the cells. I did all sorts of studies with other tissues to see if the methods I was using gave results different from those reported by others. They didn’t. Were the salts being liberated from the tissue fully before analysis? Yes. I did all the standard tricks of analytical chemistry to check that when I added a known amount to the samples I recovered that same amount during analysis. Was I making a stupid arithmetical error in calculating the concentrations? I persuaded three colleagues to work through the calculations independently; they got the same answers.

I was—and still am—at a lost to explain how Hokin found such high concentrations of all three ions of interest. However, it is interesting that her concentrations in tissue were on average 1.94 times higher; double, in other words. Richard Keynes and I concluded privately that somewhere along the line Mabel Hokin had got her sums wrong by a factor of 2. In the days before spreadsheets and even before electronic calculators came into use, the chances of systemic error were increased. Keynes himself hogged the first computer (Olivetti Programma 101) to be installed at Babraham to recalculate some figures on ion movements across an epithelium or membrane originally worked on by a co-worker. ‘Well’, he said after his marathon session, ‘they were out by a factor of 10—100 in one direction and 1000 in the other’.

After the publication of my results, I sent Mabel Hokin an offprint but I received no reply. Her ideas on how the salt gland might work were not heard of again. But why was she working on the salt gland at all?

Mabel Hokin had a very interesting personal history as well as a key role in the uncovering of a major biochemical mechanism by which signals are passed within cells, even though she did not realise it at the time.

Sir Hans (then Professor) Krebs had an enviable reputation when he was at the University of Sheffield (before his defection to Oxford) of employing school leavers as technicians and then seeing the good ones through a university degree course and postgraduate research for a PhD. A number stayed with him as fully-fledged scientists for decades, or nested successfully elsewhere. Mabel Hokin was one of those school leavers.

Mabel Hokin the 1980s
Photograph used on Wikipedia
According to a potted biography on Wikipedia. Mabel Neaverson was born in Sheffield in 1924 to working-lass parents. Throughout her life she suffered from an autoimmune disease. After spending 1942-43 in the Land Army she joined the Krebs Cell Metabolism Unit as a technician in 1943. In 1946 she became an undergraduate student (funded at least in part by Sheffield Education Committee) and in the same year married her first husband, the actor, playwright, critic and university lecturer Dennis Davison* (1923-1994); he was also at the University and they met through her interest in costume design and the theatre. Her political activities at this time in the socialist society at university (Chairman, 1947-48) and as a member, with Davison, of the Communist Party of Great Britain were to have consequences a few years later. 

After graduation in 1949 (II(i) Hons. Physiology) Krebs suggested she should continue as a research student. Her supervisor was Quentin Gibson (1918-2011, FRS 1969) then in Physiology—apparently unhappily—at Sheffield. Her PhD, funded by the Medical Research Council) was awarded in 1952. I have only found one publication from that period which shows she was working on acetate metabolism in pigeon breast muscle.

As she started her PhD, Lowell Edward Hokin (1924-2018) was arriving in Sheffield from the U.S.A., accompanied by his first wife, to work with Krebs. Then, as the Wikipedia entry reads: ‘In a short time, Mabel met Krebs' graduate student Lowell Hokin, and the two began a romantic as well as professional relationship’. Divorces were obtained; they were married in Canada in December 1952 where they had arrived from Sheffield in April.

Rather than McGill University in Montreal, they had hoped to move from Sheffield to the U.S.A. but Mabel’s entry was completely blocked during the McCarthy era because of her communist party membership. 

In experiments started at Sheffield and completed in Montreal they found that when pancreatic slices were induced to secrete digestive enzymes by cholinergic neurotransmitters, radioactive phosphorus was incorporated at a greater rate into a chemical fraction of the cell they thought was RNA. However, the radioactive label was not in RNA but in the phospholipids of the cell membranes. Until then the phospholipids were ‘regarded as inert structural components of membranes’. Later, they showed the particular phospholipids that were labelled. The Hokins were the first people to demonstrate lipid turnover caused by the stimulation of receptors on the cell. The phenomenon became known as the ‘PI effect’.

The significance of the phenomenon they had discovered was not uncovered for some years. And this is where their own work took a turn in completely in the wrong direction. Because the PI effect was apparent in other organs when stimulated to secrete, they thought that the phospholipids must be involved in transporting substances across cell membranes. Because it occurred in organs like the newly-discovered salt gland which do not secrete enzymes they argued that their phenomenon must constitute the pump which needs energy to carry sodium across cell membranes. They erected a scheme called the ‘phosphatidic acid cycle’ which, they argued, carried sodium from one side of a membrane to the other. Their hypothesis received a great deal of publicity at the time with papers in Nature and Scientific American. But then their whole scheme fell apart. All sorts of evidence accumulated to show that their phosphatidic acid cycle did not fit the bill as a transporter of ions. The world moved on. But that is how Mabel Hokin came to work on salt glands. The announcement of the discovery of salt glands by Knut Schmidt-Nielsen in 1957 coincided with the Hokins seeking an organ that secreted sodium at a high rate and that was stimulated by cholinergic nerves.

Eventually, the ban on Mabel’s admission to the U.S.A. was lifted and the Hokins had moved from Montreal to the University of Wisconsin at Madison in 1957. This is not the place to describe their later work other than to point out that they were divorced in 1971, shortly after the work on the phosphatidic acid cycle as a transport mechanism was ended and the notion shot down.

The ‘PI effect’, however, took off, as described by Bob Michell FRS in his obituary of Mabel written for Biochemist shortly after her death in 2003:

Mabel and her scientific partner and ex-husband Lowell Hokin were amongst the few scientists who have initiated a new scientific field. Their work on stimulated phosphoinositide turnover in secretory tissues, most crucially in the 1950s and 1960s, was a slow fuse that finally ignited an explosion of work that made inositol phospholipids into star players in transmembrane signalling and many other cell regulatory processes. The extraordinary versatility of phosphoinositides would have come to light at some time without their work, but it is not clear how, and it would have taken much longer… 
It took another decade for the research community to realize that the initiating event of the Hokins’ ‘PI response’ is phospholipase C-catalysed hydrolysis of PtdIns(4,5)P2, which many cell- surface receptors harness as their central signal-transducing event. Later, 3-kinase-catalysed formation of PtdIns(3,4,5)P3 emerged as a second widespread signalling reaction, and a plethora of other roles for phosphorylated derivatives of PtdIns in central cell functions have since been uncovered. 
Mabel and Lowell Hokin laid the foundations on which all of these recent discoveries stand…She and Lowell never deduced exactly what their observations meant, largely because they were doing experiments that were ‘ahead of their time’, but those of us who followed could confidently use their beautiful results to develop new interpretations. 
Mabel was a gregarious and enthusiastic woman who never lost her North Country bluntness. Even when on crutches after having new hip joints, she would be dancing at a meeting party soon after coming off a long flight…

After I first read that I felt like I had shot Bambi.

The only photograph I have found of Mabel and Lowell Hokin at about the time they were working on
salt glands. A meeting in March 1966 on the Neural Properties of Biogenuc Amines

*Davison went to Australia in 1957 eventually becoming Senior Lecturer in English at Monash University in Australia.

†Lowell Hokin died last month (6 September 2018) in Colorado.

Hokin MR. 1967. The Na+, K+ and Cl content of goose salt gland slices and the effects of acetylcholine and ouabain. Journal of General Physiology 50, 2197-2209.

Hokin MR. 1969. Electrolyte transport in the avian salt gland. In, Exocrine Glands. Proceedings of a Satellite Symposium of the XXIV International Congress of Physiological Sciences. Edited by Botelho SY, Brooks FP, Shelley WB, p 73-83. Philadelphia: University of Philadelphia Press.

Keynes RD. 1969. From frog skin to sheep rumen: a survey of transport of salts and water across multicellular structures. Quarterly Reviews of Biophysics 2, 177-281.

Kresge N, Simoni RD, Hill RL. 2005. A role for phosphoinositides in signaling: the work of Mabel R. Hokin and Lowell E. Hokin. Journal of Biological Chemistry 280, e27.

Michell R. 2003. Mabel R. Hokin (1924–2003). Biochemist, December 2003, 62-63.

Peaker M. 1971. Intracellular concentrations of sodium, potassium and chloride in the salt-gland of the domestic goose and their relation to the secretory mechanism. Journal of Physiology 213, 399-410.