Nature Genetics
20, 163 - 169 (1998)
doi:10.1038/2464
Abnormal maternal behaviour and growth retardation associated with loss
of the imprinted gene MestLouis Lefebvre1, 2, Stéphane Viville1, Sheila C. Barton1, Fumitoshi Ishino3, Eric B. Keverne4
& M. Azim Surani11
Wellcome/CRC Institute of Cancer and Developmental
Biology and Physiological Laboratory, University of Cambridge, UK.,
Tennis Court Road, Cambridge, UK, CB2 1QR
. 2
Current address: Samuel Lunenfeld Research Institute,
Mount Sinai Hospital, 600 University Avenue,
Toronto Ontario M5G 1X5, Canada. 3
Gene Research Center, Tokyo Institute of Technology
, 4259 Nagatsuta-cho, Midori-ku, Yokohama-226
, Japan. 4
Sub-Department of Animal Behaviour, University of Cambridge
, Madingley, Cambridge, UK.
Correspondence should be addressed to M. Azim Surani as10021@mole.bio.cam.ac.uk
Mest (also known as Peg1), an imprinted gene expressed only from
the paternal allele during development, was disrupted by gene targeting in
embryonic stem (ES) cells. The targeted mutation is imprinted and reversibly
silenced by passage through the female germ line. Paternal transmission activates
the targeted allele and causes embryonic growth retardation associated with
reduced postnatal survival rates in mutant progeny. More significantly,
Mest-deficient females show abnormal maternal behaviour and impaired placentophagia,
a distinctive mammalian behaviour. Our results provide evidence for the involvement
of an imprinted gene in the control of adult behaviour.
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