Insulin-like signalling to the maternal germline controls progeny response to osmotic stress.
In 1893 August Weismann proposed that information about the environment could not pass from somatic cells to germ cells, a hypothesis now known as the Weismann barrier. However, recent studies have indicated that parental exposure to environmental stress can modify progeny physiology and that parental stress can contribute to progeny disorders. The mechanisms regulating these phenomena are poorly understood. We report that the nematode Caenorhabditis elegans can protect itself from osmotic stress by entering a state of arrested development and can protect its progeny from osmotic stress by increasing the expression of the glycerol biosynthetic enzyme GPDH-2 in progeny. Both of these protective mechanisms are regulated by insulin-like signalling: insulin-like signalling to the intestine regulates developmental arrest, while insulin-like signalling to the maternal germline regulates glycerol metabolism in progeny. Thus, there is a heritable link between insulin-like signalling to the maternal germline and progeny metabolism and gene expression. We speculate that analogous modulation of insulin-like signalling to the germline is responsible for effects of the maternal environment on human diseases that involve insulin signalling, such as obesity and type-2 diabetes.
Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.
Nicholas O
NO
Burton
Department of Genetics, UT MD Anderson Cancer Center, Houston, Texas 77030, USA.
Tokiko
T
Furuta
Department of Biology Duke University, Durham, North Carolina 27708, USA.
Amy K
AK
Webster
Department of Biology Duke University, Durham, North Carolina 27708, USA.
Rebecca E W
RE
Kaplan
Department of Biology Duke University, Durham, North Carolina 27708, USA.
L Ryan
LR
Baugh
Department of Genetics, UT MD Anderson Cancer Center, Houston, Texas 77030, USA.
Swathi
S
Arur
Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.
H Robert
HR
Horvitz
D000818:Animals; D001424:Bacterial Infections / Q000473:pathology; D017173:Caenorhabditis elegans / Q000382:microbiology / Q000502:physiology*; D005854:Germ Cells / Q000378:metabolism*; D007328:Insulin / Q000378:metabolism*; D007422:Intestines / Q000196:embryology; D020935:MAP Kinase Signaling System; D009997:Osmotic Pressure; D015398:Signal Transduction; D013217:Starvation; D013312:Stress, Physiological
D007328:Insulin