GIRK2 and GABABR1 Downregulate in Response to TTX as GIRK2, GABABR1, and GABABR2 Are Not Affected by BC Treatment

Homeostatic plasticity is the response neurons undergo to regulate changes in excitability levels and bring the cells back to homeostasis. Research on homeostatic plasticity at the molecular level can lead to improved treatments for neurological diseases such as epilepsy, Alzheimer\u27s, and schizophrenia. The research featured in this poster looks at the response of GIRK (G protein-gated inwardly rectifying potassium) channels and GABAb (gamma-amniobutyric acid) receptors to neurotoxins, tetrodotoxin (TTX) or bicuculline (BC). Prolonged activity blockade of 48 hour TTX treatment significantly reduced GABABR1 and GIRK2 expression. This supports the idea that because these two proteins inhibit action potentials, there will be fewer of them found in the cell to offset the inhibition caused by TTX. However, there was no change in expression for GABABR2. In order to function, GABABR2 and GABABR1 rely on one another. Perhaps the decrease in GABABR1 expression is enough to offset the inhibition by TTX. Prolonged activity excitation of 48 hour BC treatment resulted in no significant change for GABABR1, GABABR2, and GIRK2 expressions. Although their expressions may not have changed, it is possible that their activity could still be increased

PRECS Participant: Staci Hammer

Staci Hammer, a participant in the Phenotypic Plasticity Research Experience for Community College Students, discusses her experience and assigned project

Branched chain amino acid synthesis is coupled to TOR activation early in the cell cycle in yeast

How cells coordinate their metabolism with division determines the rate of cell proliferation. Dynamic patterns of metabolite synthesis during the cell cycle are unexplored. We report the first isotope tracing analysis in synchronous, growing budding yeast cells. Synthesis of leucine, a branched-chain amino acid (BCAA), increased through the G1 phase of the cell cycle, peaking later during DNA replication. Cells lacking Bat1, a mitochondrial aminotransferase that synthesizes BCAAs, grew slower, were smaller, and were delayed in the G1 phase, phenocopying cells in which the growth-promoting kinase complex TORC1 was moderately inhibited. Loss of Bat1 lowered the levels of BCAAs and reduced TORC1 activity. Exogenous provision of BCAAs to cells lacking Bat1 promoted cell division and increased TORC1 activity. In wild-type cells, TORC1 activity was dynamic in the cell cycle, starting low in early G1 but increasing later in the cell cycle. These results suggest a link between BCAA synthesis from glucose to TORC1 activation in the G1 phase of the cell cycle.How cells coordinate their metabolism with division determines the rate of cell proliferation. Dynamic patterns of metabolite synthesis during the cell cycle are unexplored. We report the first isotope tracing analysis in synchronous, growing budding yeast cells. Synthesis of leucine, a branched-chain amino acid (BCAA), increased through the G1 phase of the cell cycle, peaking later during DNA replication. Cells lacking Bat1, a mitochondrial aminotransferase that synthesizes BCAAs, grew slower, were smaller, and were delayed in the G1 phase, phenocopying cells in which the growth-promoting kinase complex TORC1 was moderately inhibited. Loss of Bat1 lowered the levels of BCAAs and reduced TORC1 activity. Exogenous provision of BCAAs to cells lacking Bat1 promoted cell division and increased TORC1 activity. In wild-type cells, TORC1 activity was dynamic in the cell cycle, starting low in early G1 but increasing later in the cell cycle. These results suggest a link between BCAA synthesis from glucose to TORC1 activation in the G1 phase of the cell cycle