Research Article: Metabolite Profiling Uncovers Plasmid-Induced Cobalt Limitation under Methylotrophic Growth Conditions

Date Published: November 13, 2009

Publisher: Public Library of Science

Author(s): Patrick Kiefer, Markus Buchhaupt, Philipp Christen, Björn Kaup, Jens Schrader, Julia A. Vorholt, Holger Bruggemann.

Abstract: The introduction and maintenance of plasmids in cells is often associated with a reduction of growth rate. The reason for this growth reduction is unclear in many cases.

Partial Text: The term “metabolic burden” has been coined to describe the consequences of the presence and maintenance of plasmids in cells usually associated with a reduction of growth rate [1], [2], [3]. In addition to phenomena associated with overproduction of proteins that can strongly impact cell growth by consuming cellular resources or by interfering with host cell functions via its enzymatic activity or physical properties, different mechanisms are believed to account for plasmid-induced growth defects. Alterations in the physiological state of host cells transformed with plasmids, relative to the unmodified cells, are often ascribed to additional demands for ATP and precursors for DNA synthesis. This “metabolic burden” is supported by the observation that plasmid size correlates with a decrease in growth [4], [5], [6] and by a correlation between plasmid copy number and decreased growth [7], [8]. Although this is a generally accepted explanation provided by many authors, stoichiometric analyses showed that if no plasmid-encoded gene is expressed at high levels, even propagation of very high copy number vectors does not make much difference in global energy metabolism [9].



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