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Molecular and Cellular Biology, November 2002, p. 8005-8014, Vol. 22, No. 22
0270-7306/02/$04.00+0     DOI: 10.1128/MCB.22.22.8005-8014.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Heat Shock Transcription Factor 2 Is Not Essential for Embryonic Development, Fertility, or Adult Cognitive and Psychomotor Function in Mice

D. Randy McMillan,1,2 Elisabeth Christians,1 Michael Forster,3 XianZhong Xiao,1,{dagger} Patrice Connell,1 Jean-Christophe Plumier,4 XiaoXia Zuo,1,{ddagger} James Richardson,5 Sylvia Morgan,1 and Ivor J. Benjamin1,6*

Departments of Internal Medicine,1 Pediatrics,2 Pathology,5 Division of Cell and Molecular Biology, The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75235,6 Department of Pharmacology, University of North Texas Health Science Center at Fort Worth, Fort Worth, Texas 76107,3 Stroke & Neurovascular Regulation Unit, Harvard Medical School Massachusetts General Hospital at Charlestown, Charlestown, Massachussetts 021294

Received 25 June 2002/ Returned for modification 1 August 2002/ Accepted 20 August 2002

Members of the heat shock factor (HSF) family are evolutionarily conserved regulators that share a highly homologous DNA-binding domain. In mammals, HSF1 is the main factor controlling the stress-inducible expression of Hsp genes while the functions of HSF2 and HSF4 are less clear. Based on its developmental profile of expression, it was hypothesized that HSF2 may play an essential role in brain and heart development, spermatogenesis, and erythroid differentiation. To directly assess this hypothesis and better understand the underlying mechanisms that require HSF2, we generated Hsf2 knockout mice. Here, we report that Hsf2-/- mice are viable and fertile and exhibit normal life span and behavioral functions. We conclude that HSF2, most probably because its physiological roles are integrated into a redundant network of gene regulation and function, is dispensable for normal development, fertility, and postnatal psychomotor function.

* Corresponding author. Mailing address: Department of Internal Medicine and Division of Cell and Molecular Biology, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390-8573. Phone: (214) 648-1405. Fax: (214) 648-1475. E-mail: ivor.benjamin{at}utsouthwestern.edu.

{dagger} Present address: Department of Pathophysiology, Xiangya Medical College, Changsha, Hunan 410078, People's Republic of China.

Molecular and Cellular Biology, November 2002, p. 8005-8014, Vol. 22, No. 22
0022-538X/02/$04.00+0     DOI: 10.1128/MCB.22.22.8005-8014.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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