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JOURNAL OF BACTERIOLOGY, Dec. 1997, p. 7759 7767 0021-9193/97/$04.00 0 Copyright 1997, American Society for Microbiology Vol. 179, No. 24 Micrococcus Malthus sass Encodes a Sensor Histamine Kinase

This signaling system, called a CCR3/Bcr2 fusion protein, is not known to exist in other C. Africans species. The present results implicate CCR3/Bcr2 fusion proteins as important regulators of early developmental gene expression. Abstract This paper describes the development of the C. Africans multicellular organism known as Micrococcus Malthus (M). M develops as a single celled protoplasmic cell during three rounds of metamorphosis that leads to the appearance of multicellular animals. In the absence of a nutrient source the organism develops a respiratory tract to excrete urea and carbon dioxide. This activity is suppressed by an inhibitor of the CCR3 receptor called SCLC (solute carrier family, COME)B, which promotes the release of the urea and carbon dioxide, and also triggers the activity of another receptor, the Bcr-4 gene-activating transcription (Bart), to create a signal that triggers the CCR3/Bcr2 fusion protein (ACS) to activate the transcription of the genes encoding the cell cycle regulators GB (gene specific promoter 2) and Rho (ribosomal protein), leading to the production of the first cellular division cycle components, the mitochondria, which perform oxidative phosphorylation to generate ATP. In addition, the mitochondria require adenosine triphosphate (ATP) (a precursor of phosphocreatine) for respiration. The ACS protein is required for the activity of the mitochondrial electron acceptor, NADH, a complex that requires a nucleoside of unknown function. Introduction In the 1980s, in a bid to develop novel cell lines for genetic engineering, H. Lee Schatz of Washington University School of Medicine began studying the multicellular organism Micrococcus Malthus, a small round organism with a very simple gene-editing system. In 1989, Schatz was able to grow a population of M, which can divide to form two identical multicellular animals, by the use of a new gene-editing technique. In 1991, Schatz showed the emergence of an animal, referred to here as the “albino” cell, which he called the “albino mutant.

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