Research on mu heavy chain knockout mice (MuMt^-; B^null), which are mice that are genetically incapable of producing mature B-cells, has suggested that B-cells amplify the metabolic effects of diseases, especially diabetes and insulin resistance. Since type 2 diabetes (T2D) and hyperthyroidism, both of which are autoimmune conditions, are strongly correlated with PCOS, scientists have attempted to investigate an autoimmune trigger for PCOS, which has remained unsuccessful.

Study findings

In the present study, researchers evaluate previously hypothesized factors associated with cyst formation and inflammation, which include B-cell frequency, hyperandrogenemia, and autoantibodies.

A genetic editing system similar to CRISPR-Cas9 has been uncovered for the first time in eukaryotes – the group of organisms that include fungi, plants, and animals. The system, based on a protein called Fanzor, can be guided to precisely target and edit sections of DNA, and that could open up the possibility of its use as a human genome editing tool.

The research team, led by Professor Feng Zhang at the McGovern Institute for Brain Research at MIT and the Broad Institute of MIT and Harvard, began to suspect that Fanzor proteins might act as nucleases – enzymes that can chop up nucleic acids, like DNA – during a previous investigation.

They were looking into the origins of proteins like Cas9. This is the enzyme part of the CRISPR-Cas9 system. CRISPR (short for clustered regularly interspaced short palindromic repeats) sequences are the guide to particular regions of DNA, and Cas9 makes the cut. We hear a lot about CRISPR-Cas systems and their applications in medicine and biotechnology, but you may not be aware that they originate in bacteria, where they play a key role in immunity against viruses.

Plants have the unique ability to regenerate entirely from a somatic cell, i.e., an ordinary cell that does not typically participate in reproduction. This process involves the de novo (or new) formation of a shoot apical meristem (SAM) that gives rise to lateral organs, which are key for the plant’s reconstruction.

At the cellular level, SAM formation is tightly regulated by either positive or negative regulators (genes/protein molecules) that may induce or restrict shoot regeneration, respectively. But which molecules are involved? Are there other regulatory layers that are yet to be uncovered?

To seek answers to the above questions, a research group led by Nara Institute of Science and Technology (NAIST), Japan studied the process in Arabidopsis, a plant commonly used in genetic research. Their research—which was published in Science Advances —identified and characterized a key negative regulator of shoot regeneration.

Cancer spreads throughout the human body in cunning, almost militaristic, ways. For example, it can manipulate our genetic make-up, take over specific cell-to-cell signaling processes, and mutate key enzymes to promote tumor growth, resist therapies, and hasten its spread from the original site to the bloodstream or other organs.

Enzyme mutations have been of great interest to scientists who study cancer. Scientists in the Liu and Tan labs at UNC’s Lineberger Comprehensive Cancer Center have been studying mutations of enzyme recognition motifs in substrates, which may more faithfully reflect enzyme function with the potential to find new targets or directions for cancer treatment.

“We think understanding the roles of mutations on enzyme substrates, instead of the enzyme as a whole, may help to improve efficacy of targeted therapies, especially for enzymes that have both oncogenic and tumor suppressive function through controlling distinct subsets of substrates,” said Jianfeng Chen, Ph.D., who is first author and a postdoctoral fellow in the Liu lab in the UNC Department of Biochemistry and Biophysics.