es. It is also worth noting that in the absence of a large sample, researchers can use several alternative approaches to GWEIS, including: testing for GE with replicable variants identified from GWAS, including the two loci observed in the CONVERGE study2; pursuing two-stage genome-wide GE82; and conducting gene pathway-by-environment interaction analyses83 or polygenic risk score-by-environment interaction analyses8486. Several limitations should be noted. First, the outcome was based on a brief inventory of depressive symptoms during the past week, rather than levels of depressive symptoms captured over a longer period of time. Thus, it is unclear how long these symptoms lasted. However, the CES-D has demonstrated excellent psychometric properties, including in predicting DSM-IV diagnoses33,34, and its widespread use in epidemiological studies enabled us to conduct discovery and replication analyses. Future studies of trait or diagnostic measures of depressive symptoms in minority populations are needed. Second, 
the socialenvironmental exposures included in our GE analyses were based on retrospective reporting and in the case of stressful life events, only captured the prior year. Thus, our study was not designed to capture whether genetic variation interacted with stressors experienced earlier in the lifespan. Prospective studies examining GE at different stages of the lifespan are needed. Moreover, stressful life events and social support were assessed concurrently with depressive symptoms in the discovery sample as well as both replications. This may not be ideal, especially when studying the effects of stress, as prior work suggests the odds of depression is greatest in the same month of the stressor87. Longitudinal, prospective studies measuring social-environmental exposures antecedent to and close in time to depressive symptoms are necessary. These study designs are particularly important, as prior work suggests support for the 5-HTTLPR GE, for example, is more consistent when structured interviews of stressful life events are used instead of self-report questionnaires88,89. Finally, our replication samples were smaller and more phenotypically heterogeneous than the Author Manuscript Author Manuscript Author Manuscript Author Manuscript Depress Anxiety. Author manuscript; available in PMC 2017 April 01. Dunn et al. Page 12 discovery sample. For example, the WHI and HRS samples were of older adults, GTP comprised mostly middle-aged adults, and HCHS/SOL comprised a broader age range. The phenotypes also varied across these samples. Unfortunately, these limitations reflect the state of the field. Harmonizing data for GWAS and GE analyses on a large scale in racial/ethnic minority populations is challenging. Whether our failure to replicate reflects Type I error in the discovery sample or Type II error in the replication is unknown. By undertaking these analyses, we hope to spark more large-scale epidemiological studies to incorporate such measures and to study the genetic determinants of depression in women, who are more burdened by the disorder than men. During mitosis, macromolecular kinetochores assemble upon centromeric chromatin to attach chromosomes to PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19858123 spindle microtubules. In PG-490 price addition to its structural role, the kinetochore generates signals to promote proper attachment of sister chromatids to opposite spindle poles to ensure accurate segregation into daughter cells. It is unclear if the spatial distributions of mitotic kin