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Biology subjects

Mayfield, M.

Publications and source records attributed to Mayfield, M..

2 recordsLinked to original sources

The dimensionality of plant-plant competition

To avoid extinction, every species must be able to exploit available resources at least as well as the other species in its community. All else being equal, theory predicts that the more distinct the niches of such co-occurring and competing species, the more species that can persist in the long run. However, both theoretical and experimental studies define a priori the nature and number of resources over which species compete. It therefore remains unclear whether or not species in empirically realistic contexts are actually exploiting all or some of the niches available to them. Here we provide a mathematical solution to this long-standing problem. Specifically, we show how to use the interactions between sets of co-occurring plant species to quantify their implied "niche dimensionality": the effective number of resources over which those species appear to be competing. We then apply this approach to quantify the niche dimensionality of 12 plant assemblages distributed across the globe. Contrary to conventional wisdom, we found that the niche dimensionality in these systems was much lower than the number of competing species. However, two high-resolution experiments also show that changes in the local environment induce a reshuffling of plants competitive roles and hence act to increase the assemblages effective niche dimensionality. Our results therefore indicate that homogeneous environments are unlikely to be able to maintain high diversity and also shows how environmental variation impacts species niches and hence their opportunities for long-term survival.

ecology↗

PAG1 directs SRC-family kinase intracellular localization to mediate receptor tyrosine kinase-induced differentiation

All receptor tyrosine kinases (RTKs) activate similar downstream signaling pathways through a common set of effectors, yet it is not fully understood how different receptors elicit distinct cellular responses to cause cell proliferation, differentiation, or other cell fates. We tested the hypothesis that regulation of SRC Family Kinase (SFK) signaling by the scaffold protein, PAG1, influences cell fate decisions following RTK activation. We generated a neuroblastoma cell line expressing a PAG1 fragment that lacks the membrane spanning domain (PAG1-) and localized to the cytoplasm. PAG1- cells exhibited higher amounts of active SFKs and increased growth rate. PAG1- cells were unresponsive to TRKA and RET signaling, two RTKs that induce neuronal differentiation, but retained responses to EGFR and KIT. Under differentiation conditions, PAG1- cells continued to proliferate and did not extend neurites or increase {beta}-III tubulin expression. FYN and LYN were sequestered in multivesicular bodies (MVBs), and dramatically more FYN and LYN were in the lumen of MVBs in PAG1- cells. In particular, activated FYN was sequestered in PAG1- cells, suggesting that disruption of FYN localization led to the observed defects in differentiation. The results demonstrate that PAG1 directs SFK intracellular localization to control activity and to mediate signaling by RTKs that induce neuronal differentiation.

cell biology↗