Worcester Foundation for Biomedical Research

About: Worcester Foundation for Biomedical Research is a based out in . It is known for research contribution in the topics: Estrone & Estrogen. The organization has 2195 authors who have published 2646 publications receiving 115809 citations. The organization is also known as: Worcester Foundation for Experimental Biology.

The sequence of a sea urchin muscle actin gene suggests a gene conversion with a cytoskeletal actin gene.

Abstract: We report the nucleotide sequence of the single muscle actin gene of the sea urchinStrongylocentrotus purpuratus. Comparison of the protein-coding sequence of this muscle actin gene (pSpG28) with that of two linked sea urchin cytoskeletal actin genes (pSpG17 and CyIIa) reveals a region of exceptional sequence conservation from codon 61 through codon 120. Furthermore, when silent nucleotide changes are compared, the conservation of this region is still evident (7.9% silent site differences in the conserved region vs 43.3% silent site differences in the rest of the gene when pSpG28 and CyIIa are compared), indicating that the conservation is not due to particularly stringent selection on the portion of the protein encoded by this region of the genes. These observations suggest that a gene conversion has occurred between the muscle actin gene and a cytoskeletal actin gene recently in the evolution of the sea urchin genome. Gene conversion between nonallelic actin genes may thus play a role in maintaining the homogeneity of this highly conserved gene family.

Trifluoperazine-induced changes in swimming behavior of paramecium: evidence for two sites of drug action.

Abstract: Trifluoperazine (TFP), a drug that binds to Ca2+-calmodulin (CaM) complexes, altered swimming behavior not only in living paramecia, but also in reactivated, Triton-extracted "models" of the ciliate By comparing the responses of living cells and models, we have ascertained that two sites of drug action exist in paramecium cilia Swimming movements were recorded in darkfield stroboscopic flash photomicrographs; this permitted accurate quantitation of velocities and body-shape parameters When living paramecia were incubated in a standard buffer containing 10 microM TFP, their speed of forward swimming fell over several minutes and their bodies shortened Untreated paramecia backed up repeatedly and frequently upon transfer to a solution containing barium ions (the "barium dance"), but cells preincubated in TFP did not "dance" Instead they swam forward slowly for long periods of time without reversing and occasionally then exhibited abnormally prolonged reversals W7 effects on swimming mimicked low doses of TFP, and the analog W5 did not visibly alter normal swimming patterns These results suggest that TFP induces a decrease in the intracellular pCa of living paramecia, perhaps by reducing the efficiency of a calmodulin-activated calcium pump in the cell membrane Paramecia extracted with Triton X-100 and reactivated to swim forward (7 greater than or equal to pCa greater than or equal to 6) were not affected by addition of up to 40 microM TFP to the reactivation medium We conclude that the main drug effect in living cells is probably not at the axoneme However, at low pCa, TFP directly affected the ciliary axoneme to shift its behavior to one characteristic of a higher pCa: TFP inhibited backward swimming in models reactivated at pCa less than 6; instead they swam forward or rocked in place The mechanism of ciliary reversal in paramecium may therefore depend on an axonemal Ca2+-sensor, possibly bound CaM, which is affected by TFP only at low pCa, as has been postulated for other types of cilia