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Cell Immortality Gene Discovered

Science
19-FEB-98

By David Ehrenstein

For cells, aging and cancer are often opposite
sides of a genetic coin:

With "heads," cells will eventually stop dividing, reaching
a permanently quiescent stage called senescence, as
do normal human cells in lab cultures.

With "tails," the cells with genetic defects can become
immortal and never stop dividing --
a common characteristic of
cultured cancer cells.

Now, a group at Baylor College of Medicine in Houston
has found a gene that may help determine
which side the coin lands on.

Last month, at the annual meeting of the American Society
for Cell Biology, Michael Bertram reported that his
group at Baylor, led by Olivia Pereira-Smith and
James Smith, had cloned a gene that, when
mutated, helps make some types of cells
immortal.

Although researchers have identified many genes in which
mutations lead to loss of normal growth control,
at least for a number of generations, this is the
first one specifically linked to immortality.

The finding "is going to give us insights into the whole
process of [cellular] immortality," predicts
Harvey Ozer, a molecula  and cell biologist
at the New jersey Medical School
in Newark.

The Baylor team doesn't know exactly how the new gene works.

But the structure of the gene, called MORF4 (for MORtality
Factor from chromosome 4), suggests that it makes a
transcription factor, a protein that controls the
activity of other genes.

The hope is that it will be possible to track down those genes,
shedding light on both the cellular causes of immortality
and its opposite number, senescence and aging.

In addition, the work could also help provide a better
understanding of cancer, because MORF4 may
act as a tumor-suppressor gene -- one whose loss or
inactivation contributes to cancer development.

The discovery of MORF4 is an outgrowth of previous work,
in which the Baylor group and others showed that
mutations in any one of four different sets of
genes can cause cultured cells to
become immortal.

They did this by fusing various kinds of immortal cells with
either normal senescent cells or with one another.

These experiments showed that the gene defects
causing immortality are recessive:

They could be corrected by the presence of the normal gene.

The researchers also found that all of the 40 lines of immortal
cells they examined fell into four distinct groups, each
apparently having different gene mutations, because
the hybrids between members of different
groups showed normal senescence.

By fusing immortal cells with "microcells" containing only
single chromosomes, the Baylor team and others
identified chromosomes carrying the mutations,
but the amount of DNA on each chromosome
stymied their efforts to identify the
genes themselves.

They succeeded in identifying only MORF4 -- one of perhaps a
number of genes responsible for immortality in the group
designated B, which includes brain and cervical
cancer cells -- through "pure serendipity,"
Pereira-Smith says.

Two years ago, when a graduate student tried to introduce
chromosome 4 into a cell line for unrelated
experiments, only a small piece of it was
properly incorporated.

"Just for the heck of it," recalls Pereira-Smith, the student
decided to check if that small piece contained
the critical senescence gene.

To the group's surprise, putting the DNA chunk into group
B cells made them senescent, an indication that the
segment carried the normal version of a gene
whose mutation was critical to
those cells' immortality.

The Baylor team found that the piece contained five genes.

Of these, only one -- MORF4 -- caused group B cells
to become senescent, while having no
effect on other immortal cells.

They also found that the gene was up-regulated in senescent
and quiescent cells, but down-regulated
in actively dividing cells.

The researchers still do not know exactly what MORF4 does,
although they suspect it encodes a transcription factor,
because its protein product contains two "mortifs" --
a helix-loop-helix and leucine zipper -- found in
known transcription factors.

The Baylor team now hopes to find the genes this protein
might regulate and to understand their functions.

That might put them on the way to learning how cells
can live forever -- and how normal cells age.

Article Dated 18-FEB-98

COPYRIGHT 1998 American Association for the Advancement of Science

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