A Plastid-Bound Ankyrin Repeat Protein Controls Gametophyte and Early Embryo Development in Arabidopsis thaliana.

Proplastids are essential precursors for multi-fate plastid biogenesis, including chloroplast differentiation, a powerhouse for photosynthesis in plants. Arabidopsis ankyrin repeat protein (AKRP, AT5G66055) is a plastid-localized protein with a putative function in plastid differentiation and morphogenesis. Loss of function of akrp leads to embryo developmental arrest. Whether AKRP is critical pre-fertilization has remained unresolved. Here, using reverse genetics, we report a new allele, akrp-3, that exhibited a reduced frequency of mutant embryos (<13%) compared to previously reported alleles. akrp-3 affected both male and female gametophytes resulting in reduced viability, incompetence in pollen tube attraction, altered gametic cell fate, and embryo arrest that were depleted of chlorophyll. AKRP is widely expressed, and the AKRP-GFP fusion localized to plastids of both gametophytes, in isolated chloroplast and co-localized with a plastid marker in pollen and pollen tubes. Cell-type-specific complementation of akrp-3 hinted at the developmental timing at which AKRP might play an essential role. Our findings provide a plausible insight into the crucial role of AKRP in the differentiation of both gametophytes and coupling embryo development with chlorophyll synthesis.

Epigenetic targeting of transposon relics: beating the dead horses of the genome?

Transposable elements (TEs) have been seen as selfish genetic elements that can propagate in a host genome. Their propagation success is however hindered by a combination of mechanisms such as mutations, selection, and their epigenetic silencing by the host genome. As a result, most copies of TEs in a given genome are dead relics: their sequence is too degenerated to allow any transposition. Nevertheless, these TE relics often, but not always, remain epigenetically silenced, and if not to prevent transposition anymore, one can wonder the reason for this phenomenon. The mere self-perpetuating loop inherent to epigenetic silencing could alone explain that even when inactive, TE copies remain silenced. Beyond this process, nevertheless, antagonistic selective forces are likely to act on TE relic silencing. Especially, without the benefit of preventing transposition, TE relic silencing may prove deleterious to the host fitness, suggesting that the maintenance of TE relic silencing is the result of a fine, and perhaps case-by-case, evolutionary trade-off between beneficial and deleterious effects. Ultimately, the release of TE relics silencing may provide a 'safe' ground for adaptive epimutations to arise. In this review, we provide an overview of these questions in both plants and animals.