RESUMO
Contrast sensitivity was found to be better than visual acuity for predicting a pilot's ability to detect a small, semi-isolated, air-to-ground target. Eleven instructor pilots had their acuity measured by both conventional and contrast sensitivity methods. Scotopic contract sensitivity showed the highest correlation with slant detection range (0.83). Conventionally determined visual acuity proved to be a poor predictor of a pilot's ability to detect a small low contrast target.
Assuntos
Medicina Aeroespacial/métodos , Aviação , Testes Visuais/métodos , Acuidade Visual , Adulto , Aeronaves , Humanos , Masculino , Análise e Desempenho de Tarefas , Testes Visuais/instrumentaçãoRESUMO
The lin-2 gene is required for the induction of the Caenorhabditis elegans vulva. Vulval development is initiated by a signal from the anchor cell that is transduced by a receptor tyrosine kinase/Ras pathway. We show that lin-2 acts in the vulval precursor cell P6.p, downstream of lin-3 EGF and upstream of let-60 ras, to allow expression of the 1 degrees cell fate. lin-2 encodes a protein of relative molecular mass 109,000 (LIN-2A) with regions of similarity to CaM kinase II and membrane-associated guanylate kinases. Mutant lin-2 transgenes designed to lack either protein kinase or guanylate kinase activity are functional, indicating that LIN-2A has a structural rather than an enzymatic role in vulval induction. Most or all identified membrane-associated guanylate kinases are components of cell junctions, including vertebrate tight junctions and arthropod septate junctions in epithelia. Thus, LIN-2A may be a component of the cell junctions of the epithelial vulval precursor cells that is required for signaling by the receptor tyrosine kinase LET-23. We propose that LIN-2A is required for the localization of one or more signal transduction proteins (such as LET-23) to either the basal membrane domain or the cell junctions, and that mislocalization of signal transduction proteins in lin-2 mutants interferes with vulval induction.
Assuntos
Proteínas de Caenorhabditis elegans , Caenorhabditis elegans/crescimento & desenvolvimento , Caenorhabditis elegans/genética , Genes de Helmintos , Proteínas de Helminto/genética , Proteínas de Membrana/genética , Vulva/crescimento & desenvolvimento , Sequência de Aminoácidos , Animais , Sequência de Bases , Caenorhabditis elegans/metabolismo , Clonagem Molecular , Primers do DNA/genética , DNA de Helmintos/genética , Receptores ErbB/metabolismo , Feminino , Genes ras , Proteínas de Helminto/metabolismo , Junções Intercelulares/metabolismo , Proteínas de Membrana/metabolismo , Dados de Sequência Molecular , RNA Mensageiro/genética , Homologia de Sequência de Aminoácidos , Transdução de Sinais , Células-Tronco/metabolismo , Vulva/metabolismoRESUMO
In C. elegans, the anchor cell signal induces Pn.p cells to form the vulva by activating a conserved receptor tyrosine kinase pathway. lin-2 and lin-7 mutants exhibit a vulvaless phenotype similar to the phenotype observed when this signaling pathway is defective. We have found that LIN-7 is a cell junction-associated protein that binds to the LET-23 receptor tyrosine kinase. LET-23 is also localized to the cell junctions, and both LIN-2 and LIN-7 are required for this localization. LET-23 overexpression rescues the lin-2 or lin-7 vulvaless phenotype, suggesting that increased receptor density can compensate for mislocalization. These results suggest that proper localization of LET-23 receptor to the Pn.p cell junctions is required for signaling activity.