Research Sheds Light on Carbon Release During PETM

Sandra Kirtland Turner

About 56 million years ago, during an event called the Paleocene-Eocene Thermal Maximum (PETM), a large quantity of carbon was released into the atmosphere and/or oceans. This occurred naturally, but led to significant global warming, ocean acidification, and massive ecological disruption—much like the projected consequences of our current carbon release from the burning of fossil fuels.

While researchers studying the PETM agree about these fundamental characteristics, there are two critical aspects that remain debated: the amount of carbon released and the speed at which it was released. A Nature Communications article published recently by Sandra Kirtland Turner, an assistant professor of earth sciences, and her colleagues deals with the latter.

Previous estimates of the speed of carbon released during the PETM onset have varied greatly, from a few decades (perhaps due to a comet impact) to around 20,000 years. By applying novel modeling methods to analyze records of the remains of microscopic marine organisms called foraminifera, which are collected from deep sea sediment cores and provide a historic record of carbon release, Kirtland Turner demonstrates that the PETM onset likely occurred over less than 5,000 thousand years.

The title of the paper is “A Probabilistic Assessment of the Rapidity of PETM Onset.”

Postdoctoral Scholar Publishes in Stem Cell Reports

James O. Hackland, a postdoctoral scholar at UC Riverside, is the first author on a paper publishing Oct. 10 in Stem Cell Reports that focuses on the differentiation of human pluripotent stem cells (hPSCs) into neural crest cells.

The neural crest is an embryonic tissue that occurs in vertebrates and appears about three weeks into the development of the human embryo.  Soon after formation of the tissue the cells undergo a process of detachment and migration, after which their derivatives can be found throughout the body having differentiated further into a wide range of cell types that include peripheral neurons, the pigment cells of the skin (melanocytes) as well as the bone and cartilage of the face.

To date multiple publications have described the generation of neural crest cells from hPSCs. None, however, have done so in a fully-defined environment without the use of animal-derived products.

James O. Hackland


Many diseases and disorders occur as a result of defects in neural crest development, including melanoma, neuroblastoma, Hirschsprung’s disease, Waardenburg syndrome, cleft palate, Treacher Collins syndrome, and defects in the cardiac outflow tract.

“A fully defined system free of animal-derived components is required if hPSC-derived neural crest are to be used in cell replacement therapies to treat patients suffering from these serious issues,” Hackland said.  “Such a system also aids in drug discovery, and in the study of molecular signals that govern differentiation of hPSCs toward the neural crest lineage.  A necessary aspect of our work involved developing a system that controls the signaling environment of bone-morphogenetic protein, a specific growth factor.”

Hackland explained that the level of growth factor secretion by cells in culture is unpredictable and can have an adverse impact on differentiation of hPSCs.  In the research paper, he and his coauthors describe a method that controls for variation in bone-morphogenetic protein secretion that could be applied to other growth factors and have a wider impact within the field of stem cell differentiation.

Hackland, who joined UCR in late 2016, did the research as a graduate student at the University of Sheffield, the United Kingdom, and later as a postdoctoral scholar at UCR, the bulk of it at the former institution.  Currently, he works with Martin I. Garcia-Castro, an associate professor of biomedical sciences in the School of Medicine.

NIH Grant to Biomedical Scientist Will Advance Research on Inflammatory Bowel Disease

UCR Labs 2017

Earlier this year, Declan McCole, Ph.D., an associate professor of biomedical sciences in the School of Medicine, received a grant from Pfizer Inc. to explore a therapeutic target to correct intestinal barrier defects in patients with inflammatory bowel disease (IBD).  He has now received a second grant from the biopharmaceutical company to further investigate approaches to address epithelial barrier defects.

A protective protein that plays a key role in IBD is “T-cell protein tyrosine phosphatase” or TCPTP. It protects the functioning of the intestinal epithelial barrier and is encoded by a gene associated with not just IBD, but also celiac disease and type 1 diabetes.

In the earlier project, McCole’s team set out to identify how loss of expression of TCPTP leads to increased activity of a signaling pathway, called the Janus Kinase Signal Transducer and Activator of Transcription (JAK-STAT) signaling pathway, that is activated in IBD, and how this contributes to increasing intestinal barrier defects.

“We have now confirmed key roles for JAK-STAT signaling as a mediator of epithelial barrier defects in TCPTP-deficient epithelial cells,” McCole said.

The new two-year $150,000 grant will allow McCole and his team to extrapolate their cell line studies to a more translational model of the intestinal epithelium. This new model was developed with the help of a seed grant from the UCR Office of Research and Economic Development. This new award will also allow the researchers to explore a therapeutic approach to correct epithelial barrier defects by targeting JAK-STAT signaling with a drug clinically-approved to treat another chronic inflammatory condition, rheumatoid arthritis.

“We hypothesize that by reducing elevated JAK-STAT signaling we can correct barrier defects arising from loss of PTPN2 activity,” McCole said.


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