The combined functions of proapoptotic Bcl-2 family members Bak and Bax are essential for normal development of multiple tissues

Tullia Lindsten; Andrea J. Ross; Ayala King; Wei Xing Zong; Jeffrey C. Rathmell; Helena A. Shiels; Eugen Ulrich; Katrina G. Waymire; Patryce Mahar; Kenneth Frauwirth; Yifeng Chen; Michael Wei; Vicki M. Eng; David M. Adelman; M. Celeste Simon; Averil Ma; Jeffrey A. Golden; Gerard Evan; Stanley J. Korsmeyer; Grant R. MacGregor; Craig B. Thompson

doi:10.1016/S1097-2765(00)00136-2

The combined functions of proapoptotic Bcl-2 family members Bak and Bax are essential for normal development of multiple tissues

Tullia Lindsten, Andrea J. Ross, Ayala King, Wei Xing Zong, Jeffrey C. Rathmell, Helena A. Shiels, Eugen Ulrich, Katrina G. Waymire, Patryce Mahar, Kenneth Frauwirth, Yifeng Chen, Michael Wei, Vicki M. Eng, David M. Adelman, M. Celeste Simon, Averil Ma, Jeffrey A. Golden, Gerard Evan, Stanley J. Korsmeyer, Grant R. MacGregorCraig B. Thompson

Research output: Contribution to journal › Article › peer-review

1236 Scopus citations

Abstract

Proapoptotic Bcl-2 family members have been proposed to play a central role in regulating apoptosis. However, mice lacking bax display limited phenotypic abnormalities. As presented here, bak^-/- mice were found to be developmentally normal and reproductively fit and failed to develop any age-related disorders. However, when Bak-deficient mice were mated to Bax-deficient mice to create mice lacking both genes, the majority of bax^-/-bak^-/- animals died perinatally with fewer than 10% surviving into adulthood. bax^-/-bak^-/- mice displayed multiple developmental defects, including persistence of interdigital webs, an imperforate vaginal canal, and accumulation of excess cells within both the central nervous and hematopoietic systems. Thus, Bax and Bak have overlapping roles in the regulation of apoptosis during mammalian development and tissue homeostasis.

Original language	English (US)
Pages (from-to)	1389-1399
Number of pages	11
Journal	Molecular cell
Volume	6
Issue number	6
DOIs	https://doi.org/10.1016/S1097-2765(00)00136-2
State	Published - 2000
Externally published	Yes

ASJC Scopus subject areas

Molecular Biology
Cell Biology

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Lindsten, T., Ross, A. J., King, A., Zong, W. X., Rathmell, J. C., Shiels, H. A., Ulrich, E., Waymire, K. G., Mahar, P., Frauwirth, K., Chen, Y., Wei, M., Eng, V. M., Adelman, D. M., Simon, M. C., Ma, A., Golden, J. A., Evan, G., Korsmeyer, S. J., ... Thompson, C. B. (2000). The combined functions of proapoptotic Bcl-2 family members Bak and Bax are essential for normal development of multiple tissues. Molecular cell, 6(6), 1389-1399. https://doi.org/10.1016/S1097-2765(00)00136-2

Lindsten, T, Ross, AJ, King, A, Zong, WX, Rathmell, JC, Shiels, HA, Ulrich, E, Waymire, KG, Mahar, P, Frauwirth, K, Chen, Y, Wei, M, Eng, VM, Adelman, DM, Simon, MC, Ma, A, Golden, JA, Evan, G, Korsmeyer, SJ, MacGregor, GR & Thompson, CB 2000, 'The combined functions of proapoptotic Bcl-2 family members Bak and Bax are essential for normal development of multiple tissues', Molecular cell, vol. 6, no. 6, pp. 1389-1399. https://doi.org/10.1016/S1097-2765(00)00136-2

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title = "The combined functions of proapoptotic Bcl-2 family members Bak and Bax are essential for normal development of multiple tissues",

abstract = "Proapoptotic Bcl-2 family members have been proposed to play a central role in regulating apoptosis. However, mice lacking bax display limited phenotypic abnormalities. As presented here, bak-/- mice were found to be developmentally normal and reproductively fit and failed to develop any age-related disorders. However, when Bak-deficient mice were mated to Bax-deficient mice to create mice lacking both genes, the majority of bax-/-bak-/- animals died perinatally with fewer than 10% surviving into adulthood. bax-/-bak-/- mice displayed multiple developmental defects, including persistence of interdigital webs, an imperforate vaginal canal, and accumulation of excess cells within both the central nervous and hematopoietic systems. Thus, Bax and Bak have overlapping roles in the regulation of apoptosis during mammalian development and tissue homeostasis.",

author = "Tullia Lindsten and Ross, {Andrea J.} and Ayala King and Zong, {Wei Xing} and Rathmell, {Jeffrey C.} and Shiels, {Helena A.} and Eugen Ulrich and Waymire, {Katrina G.} and Patryce Mahar and Kenneth Frauwirth and Yifeng Chen and Michael Wei and Eng, {Vicki M.} and Adelman, {David M.} and Simon, {M. Celeste} and Averil Ma and Golden, {Jeffrey A.} and Gerard Evan and Korsmeyer, {Stanley J.} and MacGregor, {Grant R.} and Thompson, {Craig B.}",

note = "Funding Information: We thank the other members of the laboratories for helpful discussions and critique of the manuscript. We thank Barbi Judd for expert technical assistance and Susan Kerns for expert editorial assistance. This work was supported by grants from the National Institutes of Health, the Howard Hughes Medical Institute, and The Abramson Family Cancer Research Institute.",

year = "2000",

doi = "10.1016/S1097-2765(00)00136-2",

language = "English (US)",

volume = "6",

pages = "1389--1399",

journal = "Molecular cell",

issn = "1097-2765",

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T1 - The combined functions of proapoptotic Bcl-2 family members Bak and Bax are essential for normal development of multiple tissues

AU - Lindsten, Tullia

AU - Ross, Andrea J.

AU - King, Ayala

AU - Zong, Wei Xing

AU - Rathmell, Jeffrey C.

AU - Shiels, Helena A.

AU - Ulrich, Eugen

AU - Waymire, Katrina G.

AU - Mahar, Patryce

AU - Frauwirth, Kenneth

AU - Chen, Yifeng

AU - Wei, Michael

AU - Eng, Vicki M.

AU - Adelman, David M.

AU - Simon, M. Celeste

AU - Ma, Averil

AU - Golden, Jeffrey A.

AU - Evan, Gerard

AU - Korsmeyer, Stanley J.

AU - MacGregor, Grant R.

AU - Thompson, Craig B.

N1 - Funding Information: We thank the other members of the laboratories for helpful discussions and critique of the manuscript. We thank Barbi Judd for expert technical assistance and Susan Kerns for expert editorial assistance. This work was supported by grants from the National Institutes of Health, the Howard Hughes Medical Institute, and The Abramson Family Cancer Research Institute.

PY - 2000

Y1 - 2000

N2 - Proapoptotic Bcl-2 family members have been proposed to play a central role in regulating apoptosis. However, mice lacking bax display limited phenotypic abnormalities. As presented here, bak-/- mice were found to be developmentally normal and reproductively fit and failed to develop any age-related disorders. However, when Bak-deficient mice were mated to Bax-deficient mice to create mice lacking both genes, the majority of bax-/-bak-/- animals died perinatally with fewer than 10% surviving into adulthood. bax-/-bak-/- mice displayed multiple developmental defects, including persistence of interdigital webs, an imperforate vaginal canal, and accumulation of excess cells within both the central nervous and hematopoietic systems. Thus, Bax and Bak have overlapping roles in the regulation of apoptosis during mammalian development and tissue homeostasis.

AB - Proapoptotic Bcl-2 family members have been proposed to play a central role in regulating apoptosis. However, mice lacking bax display limited phenotypic abnormalities. As presented here, bak-/- mice were found to be developmentally normal and reproductively fit and failed to develop any age-related disorders. However, when Bak-deficient mice were mated to Bax-deficient mice to create mice lacking both genes, the majority of bax-/-bak-/- animals died perinatally with fewer than 10% surviving into adulthood. bax-/-bak-/- mice displayed multiple developmental defects, including persistence of interdigital webs, an imperforate vaginal canal, and accumulation of excess cells within both the central nervous and hematopoietic systems. Thus, Bax and Bak have overlapping roles in the regulation of apoptosis during mammalian development and tissue homeostasis.

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The combined functions of proapoptotic Bcl-2 family members Bak and Bax are essential for normal development of multiple tissues

Abstract

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