Figure 9.

Triple-localized WHY2 protein affects leaf senescence and silique development via carbon allocation. Model: (1) Overexpressing WHY2 up-regulation of NAD1 and ccb382, and down-regulation of NAD1 and ccb382 protein accumulation might lead to the interruption of mitochondrial (Mit) functional activity. (2) The nWHY2 protein in the nucleus (Nuc) directly up-regulates the expression of SWEET15 and down-regulates the expression of SWEET11, thus promoting Suc transport out of the leaf to the pericarp cells of the silique, but preventing transport of Suc derived from photosynthesis out of the chloroplast (Chl; Busi et al., 2011b), leading to an increase in starch granule numbers in chloroplasts of pericarp cells but a decline in starch content in the seed. (3) Overexpressing WHY2 in leaf cells enhances JMT and SWEET15 expression. This enhancement is up-regulated by MeJA and is consistent with the carbon reallocation in nectary cell and pollen mother cells, leading to early cell death due to carbon reallocation (Busi et al., 2011b; Cai et al., 2015). Our results suggest that WHY2 may mediates mitochondrial dysfunction, affect carbon reallocation, accelerate leaf and silique senescence, and operate on the three different plant genomes.