Figure 11.

A proposed model showing tetrapyrrole biosynthesis in mitochondria of gametophyte cells and the effect of AtHEMN1 disruption on male and female gametophyte development in Arabidopsis. LIN2 (hemF) and AtHEMN1 (hemN) convert coproporphyrinogen to protoporphyrinogen in plastids and in mitochondria, respectively. The source of uroporphyrinogen in mitochondria is currently unknown (locally synthesized or acquired from plastids) and is denoted with the dotted red arrow. We propose that the AtHEMN1 (hemN)-mediated conversion of coproporphyrinogen to protoporphyrinogen is affected in mitochondria by the Athemn1 mutation without disturbing the same in plastids. This leads to the accumulation of coproporphyrinogen and a drop in the levels of protoporphyrinogen and subsequent downstream pathway intermediates in the mitochondria in the Athemn1 mutant. Black arrows indicate normal tetrapyrrole biosynthesis in plastids and mitochondria. In mitochondria, the red solid line indicates inhibition of the conversion of coproporphyrinogen to protoporphyrinogen. Red dotted lines between protoporphyrinogen and heme indicate reduced accumulation of these products in the Athemn1 mutant. Accumulated coproporphyrinogen leads to an increased generation of ROS partly attributed to its photooxidation. The inadequate supply of heme in the mitochondria affects the synthesis of cytochrome c, affects the electron transport chain, and contributes to the generation of ROS. The ROS-mediated oxidative damage of mitochondria impairs microspore development, leading to pollen abortion. Increased ROS production in the mitochondria around the central cell of the female gametophyte prevents the fusion of polar nuclei and thereby affects ovule and seed development in Arabidopsis. UPN, Unfused polar nuclei.