Not that I was so good at keeping a secret: People at school called my friend group “The Craft,” because we seemed like we were right out of the teen witch movie. My grandmother lived by the teachings of astrologer Walter Mercado, regularly quoting him.īut for years, I mostly kept this passion quiet, for fear of what others thought. The fact that I was hardly the first in my family to explore the intuitive arts helps: My dad hails from a long line of Kabbalistic healers my great-grandmother on my mom’s side was a tarot reader in the Lower East Side of New York during the Great Depression. My parents tolerated my hobbies and my growing crystal collection. Like other witchy New Yorkers, I went shopping for white candles at Enchantments and sipped a whimsical coffee elixir at the Witches Brew in Hempstead, Long Island with friends. I had moon circles with my friends in Central Park and cast spells to elevate my GPA. I could point out every constellation, rhapsodize about every tarot card and protect my energy by sprinkling black salt. As a kid, I used to drag my parents to the local esoteric store called “Past Times” to buy crystals, incense and books.Īs a teenager, I leaned more into my interest in all things magic - it simply made the world feel more interesting. ( Plus, as a Gemini, I can't resist a story about sisters we are the twins, after all). Sally and Gillian couldn’t escape from who they were, and neither could I. 2023 21(6):e3002159.In the movie, two sisters - Sally (Sandra Bullock) and Gillian Owens (Nicole Kidman) - are introduced to their witchy heritage by their aunts, who take them in after their parents’ death. 2,3 “It will take the field still some time to sort out exactly why autophagy in myeloid cells in vivo is important for the bacterial control and inflammatory response,” said Jen Philips, a microbiologist at Washington University School of Medicine who was not involved in the study. While the researchers observed these effects in vitro using human iPSCs, others reported mixed results using mouse models. “We weren't expecting such a strong phenotype with ATG14 because there is still some autophagy operating in those cells.” In subsequent experiments, the authors found that ATG14 regulates the fusion of Mtb-containing phagosomes with lysosomes for disposal, thus identifying another mechanism by which autophagy restricts the pathogen’s escape into the cytosol. However, when they performed the same experiment in ATG14-deficient cells, the disarmed Mtb replicated successfully. As expected, wild type cells and ATG7-deficient cells showed hindered Mtb replication. Next, the researchers disarmed Mtb by deleting two defense genes. Using CRISPR-Cas9 tools, they deleted ATG7 or ATG14 from macrophages and observed increased Mtb replication in both cases, confirming that both genes are required to curtail the pathogen. Gutierrez’s team infected macrophages generated from human induced pluripotent stem cells with Mtb. Maximiliano Gutierrez, a cell biologist at The Francis Crick Institute, investigated two key genes, ATG7 and ATG14, to uncover the underlying mechanisms. Infected macrophages engage two main autophagy pathways to package Mtb into phagosomes for removal, but the exact details of how they do this are unknown. “Initial interactions are critical for disease outcomes, so understanding factors that drive pathogenic versus protective responses are really important,” said Robert Watson, a microbiologist at Texas A&M University who was not involved in the study. In a study published in Nature Microbiology, researchers probed the genetic weapons used on both sides of the battle and revealed how host cells deploy autophagy as a first line of defense to prevent Mtb from gaining a foothold. Mycobacterium tuberculosis (Mtb) and the human immune system have been at war for centuries.
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