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Reports on the living conditions of the five states seriously affected by the drought in the U.S. Feeding program of the American Red Cross for families of small owners and tenant farmers in Mississippi; Hardship of people dependent upon streams and ponds for their water in Kentucky; Part-time assistance of local agencies to the feeding and clothing of poverty-stricken people in Missouri; Unemployment among agricultural workers in Alabama; Expense of relief in Arkansas.

Discusses actions taken by Governor of Mississippi, Theodore G. Bilbo, to fulfill his political motive of obtaining a seat in the U.S. Senate, with reference to the appointment of three college presidents by him. Inefficiency of the man selected as chancellor of the University of Mississippi; Removal of faculty members and employees of A. and M. College; Information on the list of trustees and instructors who were appointed by Governor Bilbo's board; Impact of the dismissal of professors and instructors on Mississippians.

The Transforming Growth Factor-β superfamily member decapentaplegic (dpp) acts as an extracellular morphogen to pattern the embryonic ectoderm of the Drosophila embryo. To identify components of the dpp signaling pathway, we screened for mutations that act as dominant maternal enhancers of a weak allele of the dpp target gene zerknüllt. In this screen, we recovered new alleles of the Mothers against dpp (Mad) and Medea genes. Phenotypic analysis of the new Medea mutations indicates that Medea, like Mad, is required for both embryonic and imaginal disc patterning. Genetic analysis suggests that Medea may have two independently mutable functions in patterning the embryonic ectoderm. Complete elimination of maternal and zygotic Medea activity in the early embryo results in a ventralized phenotype identical to that of null dpp mutants, indicating that Medea is required for all dpp-dependent signaling in embryonic dorsal-ventral patterning. Injection of mRNAs encoding DPP or a constitutively activated form of the DPP receptor, Thick veins, into embryos lacking all Medea activity failed to induce formation of any dorsal cell fates, demonstrating that Medea acts downstream of the thick veins receptor. We cloned Medea and found that it encodes a protein with striking sequence similarity to human SMAD4. Moreover, injection of human SMAD4 mRNA into embryos lacking all Medea activity conferred phenotypic rescue of the dorsal-ventral pattern, demonstrating conservation of function between the two gene products.