Putting the MIS in Mister

As we are often painfully aware, men and women are different. Not only is this the case with our reproductive tissues, where the contrast is the most obvious, but also with many other parts of our anatomy - our body shape, amount of muscle, fat distribution, and degree of hair cover, as well as our personality and behaviour. What drives these differences between the sexes?

The journey to become either male or female begins very early in development, where differences in the production of hormones such as testosterone and oestrogen begin to kick in. In males, another hormone, Mullerian Inhibiting Substance (MIS), plays a role, masculinising the embryo by inhibiting the development of the Fallopian tubes and uterus. It has been an enduring puzzle why levels of MIS should remain high in boys until the time of puberty. Is the hormone playing an additional role as boys move toward manhood?

Previously, a team at the University of Otago, led by Associate Professor Ian McLennan discovered that MIS controls differences in the number and size of motor neurones between the sexes. Now they have been awarded a Marsden grant to investigate whether MIS plays a role in regulating the development of other sexual differences in other parts of the brain, and in tissues beyond the primary reproductive organs.

The project could lead to several important outcomes. Firstly, the confirmation of an expanded role for MIS in regulating the differences between males and females would be an important advance in developmental biology. Secondly, there would be a potential for a better understanding of drugs that affect men and women differently. Thirdly, if MIS does control differences in other parts of the brain, or in other tissues, it may help to explain why some medical conditions are more common in one particular sex – or affect men and women in different ways. For example, major depression, phobia and anorexia have a female bias; whereas men are more prone to childhood ADHD, motor neurone disease and anti-social personality disorder. A better understanding of the mechanism behind these differences might, in turn, lead to more effective treatment of these conditions.

Total Funding:    $825,000
Researchers:    Associate Professor Ian McLennan, Department of Anatomy and Structural Biology, University of Otago, Dunedin.
Associates:    Dr Kyoko Koishi, University of Otago