Interleukin-2 induces proliferation of T lymphocyte mutants lacking protein kinase C

Gordon B. Mills; Peggy Girard; Sergio Grinstein; Erwin W. Gelfand

doi:10.1016/0092-8674(88)90012-8

Interleukin-2 induces proliferation of T lymphocyte mutants lacking protein kinase C

Gordon B. Mills, Peggy Girard, Sergio Grinstein, Erwin W. Gelfand

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

146 Scopus citations

Abstract

We have identified a murine T lymphocyte clone that apparently lacks diacylglycerol- and phospholipid-activated protein kinase C (PKC): cell extracts do not display phosphatidylserine, Ca²⁺, or phorbol ester-dependent phosphotransferase activity; the enzyme was not detected in immunoblots with PKC-specific antibodies; phorbol ester binding sites are not detectable in intact cells; and activators of PKC do not stimulate proliferation or Na⁺ H⁺ exchange in intact cells. Only PKC beta mRNA was detected in normal murine T lymphocytes. The mutant T lymphocytes contained amounts of 4.4 kb PKC beta message similar to those in normal murine lymphocytes, but the 2.9 kb and 1.2 kb messages found in normal lymphocytes were barely detectable. No abnormalities were detected on Southern analysis, suggesting that the abnormality may be at the level of message splicing or stability. Since PKC-deficient cells proliferate in response to the T lymphocyte growth factor, interleukin-2, we conclude that activation of PKC is not essential for the growth-promoting action of interleukin-2.

Original language	English (US)
Pages (from-to)	91-100
Number of pages	10
Journal	Cell
Volume	55
Issue number	1
DOIs	https://doi.org/10.1016/0092-8674(88)90012-8
State	Published - Oct 7 1988
Externally published	Yes

ASJC Scopus subject areas

General Biochemistry, Genetics and Molecular Biology

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10.1016/0092-8674(88)90012-8

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title = "Interleukin-2 induces proliferation of T lymphocyte mutants lacking protein kinase C",

abstract = "We have identified a murine T lymphocyte clone that apparently lacks diacylglycerol- and phospholipid-activated protein kinase C (PKC): cell extracts do not display phosphatidylserine, Ca2+, or phorbol ester-dependent phosphotransferase activity; the enzyme was not detected in immunoblots with PKC-specific antibodies; phorbol ester binding sites are not detectable in intact cells; and activators of PKC do not stimulate proliferation or Na+ H+ exchange in intact cells. Only PKC beta mRNA was detected in normal murine T lymphocytes. The mutant T lymphocytes contained amounts of 4.4 kb PKC beta message similar to those in normal murine lymphocytes, but the 2.9 kb and 1.2 kb messages found in normal lymphocytes were barely detectable. No abnormalities were detected on Southern analysis, suggesting that the abnormality may be at the level of message splicing or stability. Since PKC-deficient cells proliferate in response to the T lymphocyte growth factor, interleukin-2, we conclude that activation of PKC is not essential for the growth-promoting action of interleukin-2.",

author = "Mills, {Gordon B.} and Peggy Girard and Sergio Grinstein and Gelfand, {Erwin W.}",

note = "Funding Information: We thank Drs. Paetkau and Havelle for providing the 2.8.2.1 cell line, Dr. Nisbet-Brown for supplying the KLH4B cell line, and Martha McGill, Mary Hill, and Chris May for technical assistance. We would like to thank P Laraya and Dr. Ian Dubefor performing the karyotype analysis. We would like to thank Dr. J. F. Kuo for assistance with the PKC immunoblots. G. 8. M. is a Medical Research Council for Canada Scholar and a McLaughlin Foundation Scientist. S. G. is a Medical Research Council of Canada Scientist. E. W. G. is a scholar of the Raymond and Beverly Sackler Foundation. This research was supported by grants from the Medical Research Council of Canada, the National Cancer Institute of Canada, and by USPHS Research grants CA-36777, HL-15696, and NS-17608 to J. F. K.",

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AU - Mills, Gordon B.

AU - Girard, Peggy

AU - Grinstein, Sergio

AU - Gelfand, Erwin W.

N1 - Funding Information: We thank Drs. Paetkau and Havelle for providing the 2.8.2.1 cell line, Dr. Nisbet-Brown for supplying the KLH4B cell line, and Martha McGill, Mary Hill, and Chris May for technical assistance. We would like to thank P Laraya and Dr. Ian Dubefor performing the karyotype analysis. We would like to thank Dr. J. F. Kuo for assistance with the PKC immunoblots. G. 8. M. is a Medical Research Council for Canada Scholar and a McLaughlin Foundation Scientist. S. G. is a Medical Research Council of Canada Scientist. E. W. G. is a scholar of the Raymond and Beverly Sackler Foundation. This research was supported by grants from the Medical Research Council of Canada, the National Cancer Institute of Canada, and by USPHS Research grants CA-36777, HL-15696, and NS-17608 to J. F. K.

PY - 1988/10/7

Y1 - 1988/10/7

N2 - We have identified a murine T lymphocyte clone that apparently lacks diacylglycerol- and phospholipid-activated protein kinase C (PKC): cell extracts do not display phosphatidylserine, Ca2+, or phorbol ester-dependent phosphotransferase activity; the enzyme was not detected in immunoblots with PKC-specific antibodies; phorbol ester binding sites are not detectable in intact cells; and activators of PKC do not stimulate proliferation or Na+ H+ exchange in intact cells. Only PKC beta mRNA was detected in normal murine T lymphocytes. The mutant T lymphocytes contained amounts of 4.4 kb PKC beta message similar to those in normal murine lymphocytes, but the 2.9 kb and 1.2 kb messages found in normal lymphocytes were barely detectable. No abnormalities were detected on Southern analysis, suggesting that the abnormality may be at the level of message splicing or stability. Since PKC-deficient cells proliferate in response to the T lymphocyte growth factor, interleukin-2, we conclude that activation of PKC is not essential for the growth-promoting action of interleukin-2.

AB - We have identified a murine T lymphocyte clone that apparently lacks diacylglycerol- and phospholipid-activated protein kinase C (PKC): cell extracts do not display phosphatidylserine, Ca2+, or phorbol ester-dependent phosphotransferase activity; the enzyme was not detected in immunoblots with PKC-specific antibodies; phorbol ester binding sites are not detectable in intact cells; and activators of PKC do not stimulate proliferation or Na+ H+ exchange in intact cells. Only PKC beta mRNA was detected in normal murine T lymphocytes. The mutant T lymphocytes contained amounts of 4.4 kb PKC beta message similar to those in normal murine lymphocytes, but the 2.9 kb and 1.2 kb messages found in normal lymphocytes were barely detectable. No abnormalities were detected on Southern analysis, suggesting that the abnormality may be at the level of message splicing or stability. Since PKC-deficient cells proliferate in response to the T lymphocyte growth factor, interleukin-2, we conclude that activation of PKC is not essential for the growth-promoting action of interleukin-2.

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Interleukin-2 induces proliferation of T lymphocyte mutants lacking protein kinase C

Abstract

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