The T-cell protein tyrosine phosphatase (TCPTP/ PTPN2) targets a broad variety of substrates across different subcellular compartments. In spite of that, the structural basis for the regulation of TCPTP's activity remains elusive. Here, we investigated whether the activity of TCPTP is regulated by a potential allosteric site in a comparable manner to its most similar PTP family member (PTP1B/PTPN1). We determined two crystal structures of TCPTP at 1.7 and 1.9 Å resolutions that include helix α7 at the TCPTP C-terminus. Helix α7 has been functionally characterized in PTP1B and was identified as its allosteric switch. However, its function is unknown in TCPTP. Here, we demonstrate that truncation or deletion of helix α7 reduced the catalytic efficiency of TCPTP by ∼4-fold. Collectively, our data supports an allosteric role of helix α7 in regulation of TCPTP's activity, similar to its function in PTP1B, and highlights that the coordination of helix α7 with the core catalytic domain is essential for the efficient catalytic function of TCPTP.

Recently, several genome-wide association studies of educational attainment have found education-related genetic variants and enabled the integration of human inheritance into social research. This study incorporates the newest education polygenic score (Lee et al. 2018) into sociological research, and tests three gene-environment interaction hypotheses on status attainment. Using the Health and Retirement Study (N = 7,625), I report three findings. First, a standard deviation increase in the education polygenic score is associated with a 60% increase in the likelihood of advancing to the next level of education, while a standard deviation increase in parental education results in a 68% increase. Second, supporting the Saunders hypothesis, the genetic effect becomes 11% smaller when parental education is one standard deviation higher, indicating that highly educated parents are more able to preserve their family's elite status in the next generation. Finally, the genetic effect is slightly greater for the younger cohort (1942~59) than the older cohort (1920~41). The findings strengthen the existing literature on the social influences in helping children achieve their innate talents.

Recently, several genome-wide association studies of educational attainment have found education-related genetic variants and enabled the integration of human inheritance into social research. This study incorporates the newest education polygenic score (Lee et al. 2018) into sociological research, and tests three gene-environment interaction hypotheses on status attainment. Using the Health and Retirement Study (N = 7,625), I report three findings. First, a standard deviation increase in the education polygenic score is associated with a 60% increase in the likelihood of advancing to the next level of education, while a standard deviation increase in parental education results in a 68% increase. Second, supporting the Saunders hypothesis, the genetic effect becomes 11% smaller when parental education is one standard deviation higher, indicating that highly educated parents are more able to preserve their family’s elite status in the next generation. Finally, the genetic effect is slightly greater for the younger cohort (1942~59) than the older cohort (1920~41). The findings strengthen the existing literature on the social influences in helping children achieve their innate talents.

Cognitive ability is one of the most potent and contentious human traits. Many issues surrounding cognitive ability especially those related to heredity is highly charged. Yet, all of the discussion on heredity has been based on non-DNA evidence. It is largely neglected that DNA and environmental data at individual level are indispensable for understanding the development of cognitive ability. In this article, we report findings from a study that uses both ability-related polygenic scores (PGSs) and a rich set of socioeconomic measures from Add Health. In an all-ethnicity sample excluding blacks, a social-science model predicts verbal ability well yielding an R2 of 17.5%. Adding two ability-related PGSs increases this R2 by 1.7%. Such models yield more accurate estimates of the effects of the PGSs and those of SES context, and provide an estimated degree to which SES context is influenced by parental genomes. Schooling and neighborhood remain important to verbal ability even after an early measure of verbal ability is adjusted in the model. Although the influence from the genome is evident, the influences of SES context are critical and cannot be dismissed.

No abstract