The intrinsically disordered N-terminal region of mouse DNA polymerase alpha mediates its interaction with POT1a/b at telomeres.

Mouse telomerase and the DNA polymerase alpha-primase complex elongate the leading and lagging strands of telomeres, respectively. To elucidate the molecular mechanism of lagging strand synthesis, we investigated the interaction between DNA polymerase alpha and two paralogs of the mouse POT1 telomere-binding protein (POT1a and POT1b). Yeast two-hybrid analysis and a glutathione S-transferase pull-down assay indicated that the C-terminal region of POT1a/b binds to the intrinsically disordered N-terminal region of p180, the catalytic subunit of mouse DNA polymerase alpha.

Search for factors contributing to resistance to the electroconvulsive seizure treatment model using adrenocorticotrophic hormone-treated mice.

Approximately one third of patients with depression remain treatment resistant with existing antidepressants, suggesting that the currently-available antidepressants cannot induce appropriate responses in the brains of all patients. Long-term exposure to adrenocorticotrophic hormone (ACTH) has been proposed as a model that mimics at least some aspects of clinical treatment-resistant depression in rodents. The purpose of this study was to explore potential causes of antidepressant treatment resistance using the chronic ACTH-treated mouse model.