The Brugge lab has shown that the calcium channel protein, TRPA1, aids in tumor survival and has proposed targeting this protein as a potential cancer treatment. In a recent publication in Cancer Cell, the Brugge lab shows how TRPA1, normally used by humans as a sensor for environmental irritants such as wasabi or spicy mustard, is co-opted by tumor cells. Some cancers express TRPA1 in high levels, creating a defense mechanism against reactive oxygen species (ROS), thereby inhibiting programmed cell death and making cancer cells less vulnerable to radiation and chemotherapy. This research adds to a growing body of evidence that cancer cell survival can be improved by anti-oxidants. By further elucidating the biological mechanisms of TRPA1 function, the Brugge lab hopes to gain a better understanding of how this protein could be targeted in clinical cancer treatments. To learn more, visit HMS news.
Dr. Steve Liberles was one of only 19 researchers across the country who were named 2018 HHMI Investigators. He has made groundbreaking discoveries in the area of neural sensory systems, with his most research focused on the role of the vagus nerve and the many basic bodily functions it regulates, including breathing, satiety, and blood pressure. Read more about his research here. Overall, the 2018 Investigator class was well-represented by Cell Biology alums; other awardees include Dr. Gia Voeltz (former Rapoport lab postdoc) and Samara Reck-Peterson (former Cell Bio faculty member).
Congratulations to Steve, Gia, and Sam!
Alban Ordureau, a postdoc in the Harper lab, has developed a proteomics method that allows for the dynamics of PARKIN-dependent mitochondrial ubiquitylation to be followed with unprecedented preision and in a site-specific manner. The approach employed targeted proteomics of ubiquitylation sites in 15 PARKIN targets, allowing digital snapshots of PARKIN activity. This system was used to monitor PARKIN activity in stem cell-derived cortical and dopaminergic neurons, and to examine mechanistic aspects of the pathway.
The Kirchhausen lab, in collaboration with Nobel laureate and Janelia group leader Eric Betzig, has developed a microscope capable of capturing 3-D images and videos of cells inside living organisms in unprecedented detail. To enable such high resolution images, researchers combined two technologies: lattice light sheet microscopy, which Betzig developed in the early 2010s, and adaptive optics, a technique borrowed from astronomy. This work was published in a new study in the April 20, 2018 issue of Science. To learn more, read here.
Dr. Wade Harper, Chair of Cell Biology and the Bert and Natalie Vallee Professor of Molecular Pathology, was just named a 2018 Fellow of the American Academy of Arts and Sciences. The mission of the Academy is to champion scholarship, civil dialogue, and useful knowledge. It is one of the country’s oldest learned societies and independent policy research centers, and it convenes leaders from the academic, business, and government sectors to respond to the challenges facing the nation and the world. Other notables named to this year's class include several Harvard-affiliated researchers, as well as Barack Obama and Sonia Sotomayor! Congrats to Wade!
Dr. Yang Shi, Merton Bernfield Professor of Neonatology at Boston Children's Hospital and Professor of Cell Biology at HMS, was appointed the C.H. Waddington Professor of Pediatrics, effective January 1, 2018. This endowed chair appointment was bestowed by the Dean of the Faculty of Medicine at HMS, with advice of the Trustees of Boston Children's hospital. Congratulations Yang!
Nick Bodnar, an MD/PhD student from the Rapoport lab, was one of 13 graduate students selected to receive a 2018 Harold M. Weintraub Graduate Student Award, which recognizes outstanding achievement in graduate studies in the biological sciences. Winners were selected based on the quality, originality, and significance of their work. Nick is a member of the HMS Biological and Biomedical Sciences graduate program. Congratulations Nick!
In a short movie produced by HMS' Office of Communications and External Relations, Fred Goldberg reminisces about his remarkable career--touching on the excitement of research, his trainees and colleagues, and the payoffs of asking basic, fundamental biological questions.
Robert Farese and Tobias Walter have an in-depth conversation on their unique scientific partnership, and the wide-ranging disease and treatment implications of lipid metabolism, in the most recent episode (“Fundamental Questions”) of The Harvard School of Public Health’s podcast Harvard Chan: This Week in Health.
Photo credit: Kent Dayton/Harvard Chan
Ribosomes are abundant cellular machines regulated by assembly, supernumerary subunit turnover, and nascent chain quality control mechanisms. Moreover, nitrogen starvation in yeast has been reported to promote selective ribosome delivery to the vacuole in an autophagy conjugation system-dependent manner, a process called "ribophagy". However, whether ribophagy in mammals is selective or regulated has not been examined. Using Ribo-Keima flux reporters, Heeseon An from the Harper lab, in a recent lab report in Nature Cell Biology, found that starvation or mTOR inhibition promotes VPS34-dependent ribophagic flux, which unlike yeast, is largely ATG8 conjugation independent and occurs concomitantly with other cytosolic protein autophagic flux reporters, indicating the absence of selectivity in this process. Ribophagic flux was not induced upon inhibition of translational elongation or nascent chain uncoupling, but was induced in a comparatively selective manner upon proteotoxic stress via arsenite or chromosome mis-segregation dependent upon VPS34 and ATG8 conjugation. Unexpectedly, Heeseon found that agents typically used to induce selective autophagy also promoted increased ribosome and cytosolic protein reporter flux, suggesting significant bulk or "by-stander" autophagy during what is often considered selective autophagy. These results emphasize the importance of monitoring non-specific cargo flux when assessing selective autophagy pathways.