Scientists at the University of Bonn have discovered a previously
unknown fruit fly gene that controls the metabolism of fat. Larvae in
which this gene is defective lose their entire fat reserves. Therefore
the researchers called the gene ‘schlank’ (German for ‘slim’). Mammals
carry a group of genes that are structurally very similar to ‘schlank’.
They possibly take on a similar function in the energy metabolism. The
scientists therefore have hopes in new medicines with which obesity
could be fought.
If scientists decipher the function of a gene, they are allowed to
name it. With the fruit fly Drosophila there is a rather paradox
convention. The names always indicate what the fly looks like if the
respective gene is defective. That is also the case with the schlank
gene. If it is unimpaired the fly larva can build up fat reserves. It
becomes fat. ‘Larvae with a mutation of schlank, however, remain slim,’
Professor Michael Hoch from the University of Bonn explains. ‘In extreme
cases the defect can even lead to death.’
Together with Dr. Reinhard Bauer and other employees the development
biologist has explored what exactly ‘schlank’ does. According to their
research the gene contains the instructions of what is known as ceramide
synthase. Ceramides serve as raw materials for the gauzy membranes that
enclose all of the cells in the body. Moreover, schlank also has a
regulatory function. It promotes lipid synthesis and at the same time
inhibits the mobilisation of fat from the fat reserves.
Mouse gene saves fly larvae
There is a chance that this is not only the case in fruit flies.
Humans also produce ceramide synthases however not just one as Drosophila
does but rather as many as six different ones. For this purpose
humans rely on a group of genes so-called Lass genes. Ceramide synthases
are extremely important for animals. Mutations in the corresponding
genes lead to severe metabolic disorders and to malfunctions of organ
systems. That is why our Lass genes look surprisingly similar to the
schlank gene of fruit flies.
This resemblance is so striking that Lass genes from mice can
partially compensate for the defect schlank gene in mutant flies. ‘We
introduced a mouse Lass gene in mutant Drosophila larvae,’
Michael Hoch says. ‘Normally the larvae died immediately after hatching.
Thanks to the Lass gene they resumed building up body fat and survived
until the next development stage.’
Up to now, the Lass genes of mammals have not been connected with the
regulation of the lipid metabolism. ‘But due to the strong parallels
with schlank we think such a function is very probable,’ Professor Hoch
presumes. ‘If this is the case they would be a promising approach for
new medications for obesity.
Source : University of Bonn