The Relationship Between Early Life Adversity and Academic Competence in Early Childhood.

It is well-documented that early life adversity negatively affects children academically and that these impacts magnify as the number of negative life events (NLEs) they experience increases. However, it is unclear whether the types of NLEs children are exposed to differentially relate to their levels of academic competence, a component of educational functioning. The present study addressed this question by assessing the relationships between different types of early life adversity and academic competence in 4- to 6-year-olds (N = 111) using secondary data analyses of parent reports in which respondents indicated children's levels of academic competence and exposure to NLEs. The results showed that family turmoil (b = -2.31, 95% CI [-4.05, -0.57], p = .01, f2 = .07), poverty (b = -2.92, 95% CI [-4.31, -1.53], p < .001, f2 = .16), and violence (b = -3.43, 95% CI [-5.14, -1.73], p < .001, f2 = .15) negatively predicted academic competence, whereas family separation and death/illness did not relate to academic competence. Additionally, poverty negatively predicted academic competence above and beyond family turmoil and violence (b = -2.36, 95% CI [-0.49, 0.72], p = .03, f2 = .04). These findings demonstrate that some, but not all, types of NLEs negatively predict preschoolers' academic competence, illustrating the differential relationship between different types of early life adversity and academic performance. Moreover, these findings reveal the deleterious impacts of certain types of NLEs on children's academics prior to beginning formal education, suggesting the importance of early intervention targeting family turmoil, poverty, and violence from a young age.

Regulation of mixed-lineage kinase activation in JNK-dependent morphogenesis.

Normal cells respond appropriately to various signals, while sustaining proper developmental programs and tissue homeostasis. Inappropriate signal reception, response or attenuation, can upset the normal balance of signaling within cells, leading to dysfunction or tissue malformation. To understand the molecular mechanisms that regulate protein-kinase-based signaling in the context of tissue morphogenesis, we analyzed the domain requirements of Drosophila Slpr, a mixed-lineage kinase (MLK), for Jun N-terminal kinase (JNK) signaling. The N-terminal half of Slpr is involved in regulated signaling whereas the C-terminal half promotes cortical protein localization. The SH3 domain negatively regulates Slpr activity consistent with autoinhibition via a conserved proline motif. Also, like many kinases, conserved residues in the activation segment of the catalytic domain regulate Slpr. Threonine 295, in particular, is essential for function. Slpr activation requires dual input from the MAP4K Misshapen (Msn), through its C-terminal regulatory domain, and the GTPase Rac, which both bind to the LZ-CRIB region of Slpr in vitro. Although Rac is sufficient to activate JNK signaling, our results indicate that there are Slpr-independent functions for Rac in dorsal closure. Finally, expression of various Slpr constructs alone or with upstream activators reveals a wide-ranging response at the cell and tissue level.