Julian Field

In 1927, the eminent art historian Erwin Panofsky published an article about linear perspective, the history of its use in paintings, the principles underlying constructions and whether perspective could be regarded as a ‘symbolic form’, that is, as a subject in itself. Today his article, which is still widely read among historians of art, seems inadequate in several ways, notably in its treatment of what would now be regarded as the relevant mathematics and optics, and some matters of history of art; moreover, to today’s readers the article also raises questions not only about how the treatment of history of the sciences has developed in the last century but also about what we would now consider an acceptable approach to writing on perspective, a subject that does not wholly belong to either history of science or to history of art.

This completes what I think one may state and defend on physical grounds concerning the foundations of Astrology and the coming year 1602. If those learned in matters of Physics think them worthy of consideration, and communicate to me their objections to them, for the sake of eliciting the truth, I shall, if God grants me the skill, reply to them in my prognostication for the following year. I urge all who make a serious study of philosophy to engage in this contest. For it concerns our worship of God and the welfare of the human race. Meanwhile, I pray from the depths of my soul, through Christ our mediator, that for all and for each the coming year may be a very happy one.

Filopodia are dynamic F-actin structures that cells use to explore their environment. c-Abl tyrosine kinase promotes filopodia during cell spreading through an unknown mechanism that does not require Cdc42 activity. Using an unbiased approach, we identified Dok1 as a specific c-Abl substrate in spreading fibroblasts. When activated by cell adhesion, c-Abl phosphorylates Y361 of Dok1, promoting its association with the Src homology 2 domain / SH3 adaptor protein Nck. Each signaling component was critical for filopodia formation during cell spreading, as evidenced by the finding that mouse fibroblasts lacking c-Abl, Dok1, or Nck had fewer filopodia than cells reexpressing the product of the disrupted gene. Dok1 and c-Abl stimulated filopodia in a mutually interdependent manner, indicating that they function in the same signaling pathway. Dok1 and c-Abl were both detected in filopodia of spreading cells, and therefore may act locally to modulate actin. Our data suggest a novel pathway by which c-Abl transduces signals to the actin cytoskeleton through phosphorylating Dok1 Y361 and recruiting Nck.