Abstract
Pentatricopeptide repeat (PPR) proteins are mainly involved in regulating post-transcriptional processes in mitochondria and plastids, including chloroplasts. Mutations in the Arabidopsis
PPR2
gene have previously been found to cause defects in seed development and reduced transmission through male and female gametophytes. However, the exact function of AtPPR2 has not been defined. We found that a loss-of-function mutation of
AtPPR2
leads to arrest of the first mitotic division during both male and female gametogenesis. In addition, the
Atppr2
mutation causes delayed embryogenesis, leading to embryonic lethality. Mutation in
emb2750
, which appears to be a weak mutant allele of the
AtPPR2
locus, also results in defective seeds. However, a majority of
emb2750
seeds were able to germinate, but their cotyledons were albino and often deformed, and growth of the
emb2750
seedlings were arrested after germination.
AtPPR2
is mainly expressed in plant parts that undergo cell division, and AtPPR2 protein was localized to chloroplasts. RNA immunoprecipitation and protein gel mobility shift assays showed that AtPPR2 binds to plastid 23S rRNA. Our study adds to a growing body of evidence that plastids and/or chloroplasts play a key role in cell division. AtPPR2 may modulate the translational process to fine-tune plastid function, thereby regulating cell division.