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Title: Drugs affecting prelamin A processing: Effects on heterochromatin organization

Journal Article · · Experimental Cell Research
; ; ;  [1];  [1]; ;  [2];  [3];  [1];  [4];  [1]
  1. IGM-CNR, Unit of Bologna, c/o IOR, Via di Barbiano 1/10 I-40136 Bologna (Italy)
  2. Department of Anatomy and Histology, University of Modena and Reggio Emilia, Modena (Italy)
  3. Department of Biopathology and Diagnostic Imaging, University of Rome Tor Vergata, Rome (Italy)
  4. Max F. Perutz Laboratories, Medical University of Vienna, Vienna (Austria)

Increasing interest in drugs acting on prelamin A has derived from the finding of prelamin A involvement in severe laminopathies. Amelioration of the nuclear morphology by inhibitors of prelamin A farnesylation has been widely reported in progeroid laminopathies. We investigated the effects on chromatin organization of two drugs inhibiting prelamin A processing by an ultrastructural and biochemical approach. The farnesyltransferase inhibitor FTI-277 and the non-peptidomimetic drug N-acetyl-S-farnesyl-L-cysteine methylester (AFCMe) were administered to cultured control human fibroblasts for 6 or 18 h. FTI-277 interferes with protein farnesylation causing accumulation of non-farnesylated prelamin A, while AFCMe impairs the last cleavage of the lamin A precursor and is expected to accumulate farnesylated prelamin A. FTI-277 caused redistribution of heterochromatin domains at the nuclear interior, while AFCMe caused loss of heterochromatin domains, increase of nuclear size and nuclear lamina thickening. At the biochemical level, heterochromatin-associated proteins and LAP2{alpha} were clustered at the nuclear interior following FTI-277 treatment, while they were unevenly distributed or absent in AFCMe-treated nuclei. The reported effects show that chromatin is an immediate target of FTI-277 and AFCMe and that dramatic remodeling of chromatin domains occurs following treatment with the drugs. These effects appear to depend, at least in part, on the accumulation of prelamin A forms, since impairment of prelamin A accumulation, here obtained by 5-azadeoxycytidine treatment, abolishes the chromatin effects. These results may be used to evaluate downstream effects of FTIs or other prelamin A inhibitors potentially useful for the therapy of laminopathies.

OSTI ID:
21045931
Journal Information:
Experimental Cell Research, Vol. 314, Issue 3; Other Information: DOI: 10.1016/j.yexcr.2007.11.012; PII: S0014-4827(07)00550-2; Copyright (c) 2007 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0014-4827
Country of Publication:
United States
Language:
English

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