The physiological role of the plastidial photosynthetic complex I (formerly NAD(P)H dehydrogenase-like complex, NDH) within the electron transport chain of plants remains intriguing. While the NDH complex shares homology with complex I, a key component of the respiratory electron transport chain, electron transport rates through the NDH complex in thylakoids are relatively low. In this study, we used a structure-function approach and mutated the plastid genome-encoded ndhF gene to abolish the NdhF proton channel of the NDH complex. These mutations led to loss of plastoquinone reductase activity, indicating tight coupling between the proton and electron transfer reactions within NDH. Additionally, loss of the transverse helix of NdhF led to loss of the NDH complex, suggesting that this region of the NdhF subunit is required for complex stability. In agreement with previous studies using ndh knockout mutants, loss of NDH complex activity did not result in measurable changes in rates of steady-state cyclic electron flow. However, all mutants displayed a shift in the sensitivity of pH-dependent feedback regulation of the photosystem II antennae to total protonmotive force (pmf), indicating a possible defect in either stromal redox state or pmf distribution into ΔpH and Δψ.
Inositol phosphates (InsP) play diverse signaling roles in regulating development, phosphate sensing, and energy metabolism. Here, we identify four maize (Zea mays) mutants, big embryo 2 (bige2), big embryo 3 (bige3), big embryo 4 (bige4), and low phytic acid 1 (lpa1), that show enlargement of the embryo at the expense of endosperm. Bige2 (identical to Lpa2), Bige3 (identical to Lpa3), and Bige4 genes encode inositol phosphate triphosphokinase (ITPK) and mono-inositol phosphate kinase (MIK), both of which catalyze lipid-independent InsP biosynthesis, and inositol polyphosphate kinase (IPK2) in the lipid-dependent InsP pathway, respectively. Lpa1 encodes a tonoplast InsP6 transporter. InsP pathway mutants primarily affect scutellum growth with each mutant exhibiting a distinct spatial pattern of cell enlargement and/or cell number. Genetic epistasis and transcriptome analyses reveal overlapping and non-redundant roles of lipid-independent and -dependent pathways in regulation of embryo development. Strikingly, ectopic expression of endosperm-specific genes in lpa2-bige2 and bige4 embryos reveals a shift toward endosperm organ identity. We identify a network of NAC transcription factors implicated in shaping lpa2-bige2 and bige4 transcriptomes. Disruption of lipid-independent InsP biosynthesis in lpa2-bige2 is associated with upregulation of a subnetwork of SOG1-related NAC proteins linked to DNA damage repair and endoreduplication. The lpa2-bige2 phenotype is fully suppressed by lpa1, suggesting that a block in InsP6 uptake into the vacuole restores signaling by cytosolic InsP intermediates. Together these results establish a genetic framework for dissecting complex roles of InsP signaling in seed development.
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：