CONTEXT: Despite their important influence on child health, it is assumed that fathers are less likely than mothers to participate in pediatric obesity treatment and prevention research. OBJECTIVE: This review investigated the involvement of fathers in obesity treatment and prevention programs targeting children and adolescents (0-18 years). DATA SOURCES: A systematic review of English, peer-reviewed articles across 7 databases. Retrieved records included at least 1 search term from 2 groups: "participants" (eg, child*, parent*) and "outcomes": (eg, obes*, diet*). STUDY SELECTION: Randomized controlled trials (RCTs) assessing behavioral interventions to prevent or treat obesity in pediatric samples were eligible. Parents must have "actively participated" in the study. DATA EXTRACTION: Two authors independently extracted data using a predefined template. RESULTS: The search retrieved 213 eligible RCTs. Of the RCTs that limited participation to 1 parent only (n = 80), fathers represented only 6% of parents. In RCTs in which participation was open to both parents (n = 133), 92% did not report objective data on father involvement. No study characteristics moderated the level of father involvement, with fathers underrepresented across all study types. Only 4 studies (2%) suggested that a lack of fathers was a possible limitation. Two studies (1%) reported explicit attempts to increase father involvement. LIMITATIONS: The review was limited to RCTs published in English peer-reviewed journals over a 10-year period. CONCLUSIONS: Existing pediatric obesity treatment or prevention programs with parent involvement have not engaged fathers. Innovative strategies are needed to make participation more accessible and engaging for fathers.

In Saccharomyces cerevisiae, silent chromatin is formed at HMR upon the passage through S phase, yet neither the initiation of DNA replication at silencers nor the passage of a replication fork through HMR is required for silencing. Paradoxically, mutations in the DNA replication processivity factor, POL30, disrupt silencing despite this lack of requirement for DNA replication in the establishment of silencing. We tested whether pol30 mutants could establish silencing at either replicated or non-replicated HMR loci during S phase and found that pol30 mutants were defective in establishing silencing at HMR regardless of its replication status. Although previous studies tie the silencing defect of pol30 mutants to the chromatin assembly factors Asf1p and CAF-1, we found pol30 mutants did not exhibit a gross defect in packaging HMR into chromatin. Rather, the pol30 mutants exhibited defects in histone modifications linked to ASF1 and CAF-1-dependent pathways, including SAS-I- and Rtt109p-dependent acetylation events at H4-K16 and H3-K9 (plus H3-K56; Miller, A., Yang, B., Foster, T., and Kirchmaier, A. L. (2008) Genetics 179, 793-809). Additional experiments using FLIM-FRET revealed that Pol30p interacted with SAS-I and Rtt109p in the nuclei of living cells. However, these interactions were disrupted in pol30 mutants with defects linked to ASF1- and CAF-1-dependent pathways. Together, these results imply that Pol30p affects epigenetic processes by influencing the composition of chromosomal histone modifications.