Unravelling the Silkworm's Genetic Fibre.

In 2004 a draft genome sequence for the silkworm was published; this makes the silkworm the member of a privileged club. Very few complicated creatures have had their complete genome sequence outlined - until recently it was a time-consuming business and only the most scientifically important animals were selected. The silkworm is a useful animal because it makes a good (large) model for other insects. It is also easy to breed and rear, is clean, quiet and sociable, and not inclined to cannibalism like, say, the spider. In other words it is the perfect house-guest and I am rather fond of them.


Since 2004 (in Chongqing Institute of Sericulture and elsewhere) this rough outline of a genome has been gradually (metaphorically) 'coloured in' to give a more accurate gene model. This is useful for many reasons. One is that the genes of an animal give a clue about its evolutionary ancestry.

For instance when the genomes of various sorts of domestic silkworms are compared with that of wild silkworms it is clear that they are genetically different. Furthermore, an analysis of the the genes shows that there was probably 'one unique event' that caused domestication, and this event happened very quickly. Just as all the races of man outside Africa come from a single mother, so all the domestic silkworms have the same wild ancestor mother. 'Just one event' - I keep thinking about this. Maybe this means that a single animal had a favourable mutation, and this has given rise to all the many millions of domestic silkworms in the world.

Before this domestication event occurred the Japanese and Chinese wild silkworm had already diverged - the genomes have revealed this too. They also reveal that these Japanese strains have subsequently been 'invaded' by the domesticated silkworm strains - that is, somewhere along the track some domesticated silkworms mated with some wild Japanese silkworms and their genes were incorporated.

The genome has also solved the puzzle of the specific diet of the silkworm which has intrigued me ever since I'd heard about it. I've already described, months ago, how Japanese scientists determined what causes the silkworm to be so fussy and only eat mulberry. (To recap the silk worm is attracted by the smell of the mulberry through antennae on the top of its head, but needs different smells from the mulberry, detected by feelers next to its mouth, before it will start chewing and swallowing. The Japanese scientists discovered this by slicing off various silkworm parts. They were elegant experiments but cruel ones).

But why should the silkworm be so fussy? The answer probably lies in the fact that to most animals the mulberry is poisonous, and so any animal that can get around this will have its own unique food source that is shirked by all others. Gradually the silkworm must have evolved alongside the mulberry and adapted to the mulberry's poison. Analysis of the genes has revealed exactly how this adaptation happened. The poison is an alkaloid, which requires a special enzyme to digest it. Until silkworms came on the scene only bacteria and some plants had this special enzyme - but now silkworms have incorporated some of the bacteria's genes into its own genome so it can make the enzyme too. I imagine some proto-silkworm might have been infected by the bacteria, and somehow, maybe by means of a virus which is good at mixing DNA (though this is just my guess-work) the genes of the cells of this proto-silkworm changed.

Apart from the genes to produce the mulberry-alkaloid-busting-enzyme the silkworm genome also contains genes that produce silk. Locating these is interesting because it enables scientists to rearrange them and maybe make them produce a more valuable protein. This has been done too. Silkworms have produced pharmaceutically-useful proteins in their silk, as well as silks of different colours, and strengths.


Apart from this, according to the abstract kindly given to me by Dr. Guoqing Pan in Chongqing, scientists have investigated the genes involved in making the pigmentation in newly hatched silkworms, how insulin is regulated, how a mutation that gives rise to yellow silkworms also causes these silkworms to die - long before they reach the pupa stage, altered the genes of silkworms so that one strain conveniently dies before it hatches out of its cocoon, and another strain that not only dies but also does not decay.

The silkworm's immune system - its genetic origins and the way it acts - were also examined. The silkworm is a useful model for other insects in particular the Lepidoptera (because it is so large and so easily examined) as well as elements of our own immune system - the innate part that has proved itself so valuable similar systems occur unaltered in all animals, even ourselves.

There were also many studies on Microspordia. Until I read these abstracts I'd never heard of Microsporidia but apparently Pebrine, the scourge of the silkworm (and discovered by Louis Pasteur), is one of them. Microsporidia are related to fungi and are the cause of some parasitic infections in children in the tropics.

Microsporidia are interesting because they have evolved from mitochondria by eliminating some of their genetic material and becoming less complicated. They have lost so many genes that they can no longer make the metabolites necessary to live - so, like viruses, they have depend on hosts for their survival. However, whereas viruses hijack the replication mechanism of the cell, the microsporidia extract nutrients. Once a spore comes into contact with a host, it is activated and a tube which has been coiled up inside the spore, is ejected with such force that it breaks through both the spore wall and the plasma membrane of the host.

Microsporidia can infect all animal groups and is an emerging human pathogen. Since it is a tropical disease, outbreaks of microsporidia infection are likely to become more frequent and widespread as the earth warms. So understanding the microsporidia genome and what the disease needs to survive and thrive is important - and once again the silkworm, or rather its disease, Pebrine, is a useful model.

Pebrine microspores, however, are slightly different from other microsporidea and have a different evolutionary history. They have bucked the genetic trend and instead of decreasing the number of their genes they have duplicated them. This has given them some adaptability and enabled them to infect a wider range of hosts. Just as the proto-silkworms incorporated some bacterial genes into its genome, so the Pebrine microspore has actually incorporated some of the genetic material of the silkworm into its genome. It is an interesting to think that such different living things combine and merge.

So this collection of abstracts describes a diverse range of discoveries, with some important implications, all generated from, or related to, a project to investigate the genome of the silkworm. No doubt the project was started for economic reasons - improving silk productivity and quality - but has subsequently broadened into unsuspected areas. That is the beauty of scientific research, and also why it is so infuriating. It takes unexpected turns, and can occasionally turn out to be more valuable than anyone could have imagined.