Kombucha, a fermented tea beverage with an acidic and effervescent taste, is composed of a multispecies microbial ecosystem with complex interactions that are characterized by both cooperation and conflict. In kombucha, a complex community of bacteria and yeast initiates the fermentation of a starter tea (usually black or green tea with sugar), producing a biofilm that covers the liquid over several weeks. This happens through several fermentative phases that are characterized by cooperation and competition among the microbes within the kombucha solution. Yeast produce invertase as a public good that enables both yeast and bacteria to metabolize sugars. Bacteria produce a surface biofilm which may act as a public good providing protection from invaders, storage for resources, and greater access to oxygen for microbes embedded within it. The ethanol and acid produced during the fermentative process (by yeast and bacteria, respectively) may also help to protect the system from invasion by microbial competitors from the environment. Thus, kombucha can serve as a model system for addressing important questions about the evolution of cooperation and conflict in diverse multispecies systems. Further, it has the potential to be artificially selected to specialize it for particular human uses, including the development of antimicrobial ecosystems and novel materials. Finally, kombucha is easily-propagated, non-toxic, and inexpensive, making it an excellent system for scientific inquiry and citizen science.

Estrogen receptor α (ERα)low/− tumors are associated with breast cancer (BCa) endocrine resistance, where ERα low tumors show a poor prognosis and a molecular profile similar to triple negative BCa tumors. Interleukin‐1 (IL‐1) downregulates ERα accumulation in BCa cell lines, yet the cells can remain viable. In kind, IL‐1 and ERα show inverse accumulation in BCa patient tumors and IL‐1 is implicated in BCa progression. IL‐1 represses the androgen receptor hormone receptor in prostate cancer cells concomitant with the upregulation of the prosurvival, autophagy‐related protein, Sequestome‐1 (p62/SQSTM1; hereinafter, p62); and given their similar etiology, we hypothesized that IL‐1 also upregulates p62 in BCa cells concomitant with hormone receptor repression. To test our hypothesis, BCa cell lines were exposed to conditioned medium from IL‐1‐secreting bone marrow stromal cells (BMSCs), IL‐1, or IL‐1 receptor antagonist. Cells were analyzed for the accumulation of ERα, progesterone receptor (PR), p62, or the autophagosome membrane protein, microtubule‐associated protein 1 light chain 3 (LC3), and for p62‐LC3 interaction. We found that IL‐1 is sufficient to mediate BMSC‐induced ERα and PR repression, p62 and autophagy upregulation, and p62‐LC3 interaction in ERα+/PR+ BCa cell lines. However, IL‐1 does not significantly elevate the high basal p62 accumulation or high basal autophagy in the ERα−/PR− BCa cell lines. Thus, our observations imply that IL‐1 confers a prosurvival ERα−/PR− molecular phenotype in ERα+/PR+ BCa cells that may be dependent on p62 function and autophagy and may underlie endocrine resistance.

Insect wing polyphenism has evolved as an adaptation to changing environments and a growing body of research suggests that the nutrient-sensing insulin receptor signalling pathway is a hot spot for the evolution of polyphenisms, as it provides a direct link between growth and available nutrients in the environment. However, little is known about the potential role of insulin receptor signalling in polyphenisms which are controlled by seasonal variation in photoperiod. Here, we demonstrate that wing length polyphenism in the water strider Gerris buenoi is determined by photoperiod and nymphal density, but is not directly affected by nutrient availability. Exposure to a long-day photoperiod is highly inducive of the short-winged morph whereas high nymphal densities moderately promote the development of long wings. Using RNA interference we demonstrate that, unlike in several other species where wing polyphenism is controlled by nutrition, there is no detectable role of insulin receptor signalling in wing morph induction. Our results indicate that the multitude of possible cues that trigger wing polyphenism can be mediated through different genetic pathways and that there are multiple genetic origins to wing polyphenism in insects.

Granulocyte Macrophage Colony Stimulating Factor (GM-CSF) is a 16.29 kDa cytokine that regulates the leukocyte production, migration and functions. The GM-CSF receptor ligand interaction stability plays vital role for prolonged differentiation of haematopoietic stem cell into granulocytes and monocytes. In the present investigation attempts were made to increase the number of stabilization centres in GM-CSF ligand using molecular simulation. This improves half-life stability of GM-CSF receptor ligand interaction complex. The numbers of stabilization centres were increased by amino-acid substitution which led to change in contact energy, hydrophobicity index and unfolding Gibbs free energy without altering receptor ligand interaction. Multiple sequence alignment of GM-CSF sequence using ClustalW with Ovies aries, Homo sapiens, Mus musculus and Gallus gallus species revealed the conserved domain regions and aminoacid dissimilarities in conserved and other regions. Based on the above, 21N, 25L, 42V, 55L, 56Q, 93E and 102T were mutated with its aminoacid substitution property. Different combinations of mutation were incorporated in the amino acid sequence and mutant proteins were modelled using structure of GM-CSF ligand (PDB ID: 1CSG) as a template by MODELLER. After mutation, the GLU21, LEU25, LEU55 and THR102 positions were identified as stability centre using SCide. Mutations at residues LEU55 and THR102 had 16.71% lesser energy value than the wild type GMCSF energy value which is 6831.73. The result suggested that, the stability of human GM-CSF has been increased (as the energy decreases) due to mutagenesis by computational tools.