Editor—Spinal muscular atrophy (SMA) is an autosomal recessive disease resulting from mutations in the telomeric copy of the survival motor neuron gene (SMN1),1-7 which results in reduced expression of the survival of motor neuron protein (SMN).4 7 The SMN protein is ubiquitously expressed but is found at high levels in motor neurons.4 7 8 The SMN protein associates with Sm proteins,9 10 SIP-1 protein,9 10 and itself.8-11 SMN is found in structures termed gems8 that are associated with coiled bodies in the nucleus. The SMN protein is involved in RNA biogenesis10 and is important for the maturation of a functional snRNP complex that performs splicing.12 The complete loss of SMN is lethal13 whereas the low levels of SMN found in SMA cause loss of the motor neurons.4 7 The mechanism by which the reduction of SMN protein results in the loss of motor neurones is unknown. Some groups have suggested it occurs by apoptosis.14 15 Apoptosis is a conserved, highly regulated mechanism of non-chronic cell death for the removal of surplus, aged, or damaged cells.15 Apoptosis is regulated by the interactions of apoptosis agonists and antagonist with the Bcl-2 protein being one of the key inhibitors of apoptosis.16

Recently Iwahashi et al 17 have suggested a direct interaction between SMN and Bcl-2 using transfected constructs. In an effort to confirm and extend their results, we have attempted to coimmunoprecipitate SMN and Bcl-2 both in a native environment and using transfected cells. The SMN protein and Bcl-2 are expressed in Jurkat cells and in spinal cord. Jurkat cells are a human lymphoblast T cell line that has been previously shown to express Bcl-2 and can be induced to undergo apoptosis.18 19

Immunoprecipitation experiments …