Microprogramming a Writeable Control Memory using Very Long Instruction Word (VLIW) Compilation Techniques

Microprogrammed Digital Signal Processors (DSP) are frequently used as a solution to embedded processor applications. These processors utilize a control memory which permits execution of the processor\u27s instruction set architecture (ISA). The control memory can take the form of a static, read only memory (ROM) or a dynamic, writeable control memory (WCM), or both. Microcoding the WCM permits redefining the processor\u27s ISA and provides speedup due to its instruction level parallelism (ILP) potential. In the past, code generation efforts for microprogrammable processors focused on creating assembly and microcode as two separate steps. In this thesis an alternative approach was chosen which combines the separate code generation steps into one automated, dual-target compilation process using the advanced techniques of VLIW compiler technology. The architecture chosen for this effort is a microprogrammable DSP being developed by Rome Labs, New York. The prototype compiler developed in this effort has demonstrated the potential for speedup of microcoded program portions over their assembly code counterparts. Therefore, the feasibility of program speedup produced by a dual-target compiler using VLIW compilation techniques has been validated

Nodal-Dependent Mesendoderm Specification Requires the Combinatorial Activities of FoxH1 and Eomesodermin

Vertebrate mesendoderm specification requires the Nodal signaling pathway and its transcriptional effector FoxH1. However, loss of FoxH1 in several species does not reliably cause the full range of loss-of-Nodal phenotypes, indicating that Nodal signals through additional transcription factors during early development. We investigated the FoxH1-dependent and -independent roles of Nodal signaling during mesendoderm patterning using a novel recessive zebrafish FoxH1 mutation called midway, which produces a C-terminally truncated FoxH1 protein lacking the Smad-interaction domain but retaining DNA–binding capability. Using a combination of gel shift assays, Nodal overexpression experiments, and genetic epistasis analyses, we demonstrate that midway more accurately represents a complete loss of FoxH1-dependent Nodal signaling than the existing zebrafish FoxH1 mutant schmalspur. Maternal-zygotic midway mutants lack notochords, in agreement with FoxH1 loss in other organisms, but retain near wild-type expression of markers of endoderm and various nonaxial mesoderm fates, including paraxial and intermediate mesoderm and blood precursors. We found that the activity of the T-box transcription factor Eomesodermin accounts for specification of these tissues in midway embryos. Inhibition of Eomesodermin in midway mutants severely reduces the specification of these tissues and effectively phenocopies the defects seen upon complete loss of Nodal signaling. Our results indicate that the specific combinations of transcription factors available for signal transduction play critical and separable roles in determining Nodal pathway output during mesendoderm patterning. Our findings also offer novel insights into the co-evolution of the Nodal signaling pathway, the notochord specification program, and the chordate branch of the deuterostome family of animals