인문학
사회과학
자연과학
공학
의약학
농수해양학
예술체육학
복합학
지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
초록·키워드
Growing evidence suggests that counter-transport of phosphatidylinositol-4-phosphate (PtdIns(4)P) and phosphatidylserine (PS) at endoplasmic reticulum (ER)-plasma membrane (PM) contact sites is required for intracellular vesicle transport. PtdIns(4)P is metabolized by Stt4 PI 4-kinase residing at the PM and by Sac1 PtdIns(4)P phosphatase at the ER, and ER-PM contact sites are believed to be important for its efficient turnover. Recently, Stt4 has been shown to extensively localize to ER-PM contact sites. However, the precise location of Stt4 and the mechanism of localization to these sites have not been clarified. Additionally, although several studies have suggested a requirement for PS/PtdIns(4)P and sterol/PtdIns(4)P exchange at ER-PM contact sites in endocytosis, it is still unclear whether contact between the ER and the PM, turnover of PtdIns(4)P or PS, or maintenance of PtdIns(4)P or PS levels is more important. Here we found that Stt4 localizes to the cER regions where Scs2 and Ist2 are localized abundantly, and that localization of Stt4 is maintained in the Δtether mutant, which has a reduced number of ER-PM contact sites. We also demonstrated that the Δtether and sac1Δ mutants showed defects at different stages of endocytosis, and that the inactivation mutation of Stt4 restored the endocytosis defect only in the Δtether mutant. Furthermore, these mutants exhibited defective transport in the secretory and recycling pathways, and inactivation of Stt4 restored the secretory pathway in the Δtether mutant, but not the recycling pathway in either mutant. These results suggest that endocytosis, secretion, and recycling pathways are regulated directly or indirectly by different PtdIns(4)P-mediated mechanisms.
인공지능 문자 인식 모델을 통해 추출된 텍스트로, 일부 오타나 오류가 포함될 수 있으나 지속적으로 개선 중입니다.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.