Depression is among the most prevalent, disabling and costly mental health conditions worldwide. Adolescence is a critical time for studying the vulnerability to depression as there is dramatically increasing risk for its onset during this period. Research has demonstrated that MAOA gene played an important role in the development of depression and maternal parenting was also tightly associated with depression. More importantly, accumulating evidence of gene-parenting interactions has been observed in recent years. However, most of these studies have largely focused on adverse rearing environments such as childhood abuse, and rarely on positive parenting. Moreover, most of them were guided by the diathesis-stress model and “risk alleles” assumption, whereas the genes could be “plasticity” rather than “risk” according to the differential susceptibility model. The present study aimed to examine the interaction between MAOA rs6323 polymorphism and maternal supportive parenting on adolescent depression, and further test these two competing models: diathesis-stress vs. differential susceptibility.

One thousand and twenty five adolescents (male = 679) from 39 classes of 14 primary schools in Jinan City were followed from grade 6 till to grade 9. Adolescent depression was accessed using Children’s Depression Inventory (CDI), and mothers were asked to report their supportive parenting (including warmth and encouragement of autonomy) via the Chinese version of Child-Rearing Practices Report (CRPR). DNA samples of adolescents were extracted from their saliva to genotype the MAOA rs6323 polymorphism. Statistically, two newly-developed approaches, RoS (regions of significance) method and re-parameterized regression models were used to examine the interaction between rs6323 polymorphism and maternal supportive parenting on adolescent depression and further test the two competing G×E hypotheses. The main findings of the present study were as follows:

The MAOA rs6323 polymorphism significantly interacted with maternal supportive parenting in predicting adolescent depression, but this interaction was only observed in females. Both maternal warmth and encouragement of autonomy negatively predicted female adolescent depression among carriers of GG homozygotes but not TT homozygotes. Moreover, the indexes in RoS method and re-parameterized regression models both provided strong support for the differential susceptibility hypothesis.

By elaborating the moderating effect of maternal supportive parenting and gender, the present study enriches the literature of the relation between MAOA gene and adolescent depression and further expands our knowledge about the G×E underpinnings of depression. Also, this study provides additional strong support for the differential susceptibility hypothesis by using RoS and re-parameterized regression methods.