What Can Cognitive Science Do for People?

The critical question for cognitive scientists is what does cognitive science do, if anything, for people? Cognitive science is primarily concerned with human cognition but has fallen short in continuously and critically assessing the who in human cognition. This complacency in a world where white supremacist and patriarchal structures leave cognitive science in the unfortunate position of potentially supporting those structures. We take it that many cognitive scientists operate on the assumption that the study of human cognition is both interesting and important. We want to invoke that importance to note that cognitive scientists must continue to work to show how the field is useful to all of humanity and reflects a humanity that is not white by default. We wonder how much the field has done, and can do, to show that it is useful not only in the sense that we might make connections with researchers in other fields, win grants and write papers, even of the highest quality, but useful in some material way to the billions of non-cognitive scientists across the globe.

Organization and evolution of multifunctional Ca(2+)/CaM-dependent protein kinase genes.

The "multi-functional" Ca(2+) and calmodulin-dependent protein kinase, type II (CaMK-II) is an evolutionarily conserved protein. It has been found as a single gene in the horseshoe crab, marine sponge, sea urchin, nematode, and fruit fly, whereas most vertebrates possess four genes (alpha, beta, gamma, and delta). Species from fruit flies to humans encode alternative splice variants which are differentially targeted to phosphorylate diverse downstream targets of Ca(2+) signaling. By comparing known CaMK-II protein and nucleotide sequences, we have now provided evidence for the evolutionary relatedness of CaMK-IIs. Parsimony analyses unambiguously indicate that the four vertebrate CaMK-II genes arose via repeated duplications. Nucleotide phylogenies show consistent but moderate support for the placement of the vertebrate delta CaMK-II as the earliest diverging vertebrate gene. delta CaMK-II is the only gene with both central and C-terminal variable domains and has three to four times more intronic sequence than the other three genes. beta and gamma CaMK-II genes show strong sequence similarity and have comparable exon and intron organization and utilization. alpha CaMK-II is absent from amphibians (Xenopus laevis) and has the most restricted tissue specificity in mammals, whereas beta, gamma, and delta CaMK-IIs are expressed in most tissues. All 38 known mammalian CaMK-II splice variants were compiled with their tissue specificity and exon usage. Some of these variants use alternative 5' and 3' donors within a single exon as well as alternative promoters. These findings serve as an important benchmark for future phylogenetic, developmental, or biochemical studies on this important, conserved, and highly regulated gene family.

Axonal localization of delta Ca2+/calmodulin-dependent protein kinase II in developing P19 neurons.

Ca(2+)/calmodulin-dependent protein kinase, type II (CaMK-II) is an enzyme encoded by four genes (alpha, beta, gamma and delta) and traditionally associated with synaptic function in the adult central nervous system, but also believed to play a role during neuronal development. P19 mouse embryonic cells are a model system for neurogenesis and primarily express isozymes of delta CaMK-II. It is not yet known whether or where delta CaMK-II is expressed in P19 neurons. Using an antibody specific for the delta CaMK-II C-terminal tail, we detected a 20-fold increase in levels of delta CaMK-II along axons after 8 days of development. This coincides with increased mRNA and protein levels of delta(C) CaMK-II, which contains the alternative tail. This follows the initial stages of neurite outgrowth and beta(3) tubulin expression, which occur after 4 days. delta CaMK-II co-localizes with the axonal protein GAP-43, but not the dendritic microtubule-associated protein MAP-2, a known substrate of alpha CaMK-II. Like delta CaMK-II, GAP-43 shows increased expression after 8 days. These findings demonstrate developmental regulation of the alternative C-terminal delta CaMK-II exon and implicate endogenous delta CaMK-II in axonal development in embryonic cells.