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Analysis of the tumor microenvironment reveals that pancreatic tumors experience metabolic stress caused by immune cell degradation of the amino acid arginine, and that pancreatic cancers cope by synthesizing arginine to provide access this amino acid despite low tumor availability.

Phenomics assays reveal hundreds of mutant phenotypes for long non-coding RNAs grown in specific environmental or physiological contexts, indicating that most of these RNAs exert cellular functions under certain conditions.

Pancreatic cancers can utilize hyaluronic acid, an abundant extracellular matrix component in the tumor microenvironment, to fuel cancer cell metabolism and growth.

The activin receptor ALK7 regulates the adaptation of brown adipose tissue to nutrient availability by preventing over-activation of signaling pathways induced by fasting, allowing appropriate response to cold exposure.

Infection with Mycobacterium tuberculosis triggers de novo synthesis of polyunsaturated fatty acids by host macrophages, which promote their antimicrobial responses but feed the intracellular pathogen.

Novel high-throughput co-culture assays reveal how the spatial structure of colony biofilms provides opportunities for nutrient and matrix sharing and may drive the evolution of cooperative behaviors.

Food supply and nutrient stress tolerance coordinately shape the multilevel selection dynamics of a mitochondrial cheater by promoting cheater persistence at both within-host and between-host levels of selection.

The ALK7 receptor functions cell-autonomously and homeostatically in adult adipocytes to regulate catecholamine sensitivity in response to the diet.

Like physical systems that exhibit nucleation phenomena, an invading population of a strong microbial antagonist requires a critical inoculum size to successfully invade a population of a weaker microbial antagonist.

CysM and CysK2 play complementary and overlapping roles in Mtb's adaptation to environmental stress that are crucial for survival.