Adolescent Involvement in Cybergossip: Influence on Social Adjustment, Bullying and Cyberbullying.

Gossip is a type of social behavior present in all types of social networks, and cybergossip is an emerging kind of online social behavior which can both promote and hinder relationships between peers. The aim of this study was to explore the relation between involvement in cybergossip and the development of behavior of social adjustment, bullying and cyberbullying (aggression and victimization), based on gender and age. A total of 510 secondary school students (49.4% girls) aged 12 to 17 years old (M = 14.01; SD = 1.38) were surveyed by self-report. Questionnaires validated with adolescents were used to measure bullying, social adjustment and cyberbullying. The results showed that a high prevalence of involvement in cybergossip was associated with bullying and cyberbullying behavior (aggression and victimization), with girls showing the greatest involvement in cybergossip. The discussion of the results focuses on the gender difference, as well as the importance of the need for training in the proper use of digital devices for social education and socialization.

MYBL2 and ATM suppress replication stress in pluripotent stem cells.

Replication stress, a major cause of genome instability in cycling cells, is mainly prevented by the ATR-dependent replication stress response pathway in somatic cells. However, the replication stress response pathway in embryonic stem cells (ESCs) may be different due to alterations in cell cycle phase length. The transcription factor MYBL2, which is implicated in cell cycle regulation, is expressed a hundred to a thousand-fold more in ESCs compared with somatic cells. Here we show that MYBL2 activates ATM and suppresses replication stress in ESCs. Consequently, loss of MYBL2 or inhibition of ATM or Mre11 in ESCs results in replication fork slowing, increased fork stalling and elevated origin firing. Additionally, we demonstrate that inhibition of CDC7 activity rescues replication stress induced by MYBL2 loss and ATM inhibition, suggesting that uncontrolled new origin firing may underlie the replication stress phenotype resulting from loss/inhibition of MYBL2 and ATM. Overall, our study proposes that in addition to ATR, a MYBL2-MRN-ATM replication stress response pathway functions in ESCs to control DNA replication initiation and prevent genome instability.