To maintain homeostasis in an ever-changing environment organisms have evolved 
mechanisms to reprogram gene expression. One central mechanism regulating gene 
expression is messenger RNA (mRNA) degradation, which is initiated by poly(A) 
tail shortening (deadenylation). The carbon catabolite repressor 4-CCR4 
associated factor1 (CCR4-CAF1) complex is the major enzyme complex that 
catalyzes mRNA deadenylation and is conserved among eukaryotes. However, the 
components and functions of this global regulatory complex have not been well 
characterized in plants. Here we investigate the CAF1 family in Arabidopsis 
(Arabidopsis thaliana). We identify 11 AtCAF1 homologs and show that a subset of 
these genes are responsive to mechanical wounding, among them are AtCAF1a and 
AtCAF1b whose expression levels are rapidly and transiently induced by wounding. 
The differential expression profiles of the various AtCAF1s suggest that not all 
AtCAF1 genes are involved in stress-responsive regulation of transcript levels. 
Comparison of misexpressed genes identified via transcript profiling of Atcaf1a 
and Atcaf1b mutants at different time points before and after wounding suggests 
that AtCAF1a and AtCAF1b target shared and unique transcripts for deadenylation 
with temporal specificity. Consistent with the AtPI4Kgamma3 transcript 
exhibiting the largest increase in abundance in Atcaf1b, AtCAF1b targets 
AtPI4Kgamma3 mRNA for deadenylation. Stress-tolerance assays demonstrate that 
AtCAF1a and AtCAF1b are involved in mediating abiotic stress responses. However, 
AtCAF1a and AtCAF1b are not functionally redundant in all cases, nor are they 
essential for all environmental stresses. These findings demonstrate that these 
closely related proteins exhibit overlapping and distinct roles with respect to 
mRNA deadenylation and mediation of stress responses.