Biogenesis of mammalian mitochondrial ribosomes requires a concerted maturation of both the small (SSU) and large subunit (LSU). We demonstrate here that the m5C methyltransferase NSUN4, which forms a complex with MTERF4, is essential in mitochondrial ribosomal biogenesis as mitochondrial translation is abolished in conditional Nsun4 mouse knockouts. Deep sequencing of bisulfite-treated RNA shows that NSUN4 methylates cytosine 911 in 12S rRNA (m5C911) of the SSU. Surprisingly, NSUN4 does not need MTERF4 to generate this modification. Instead, the NSUN4/MTERF4 complex is required to assemble the SSU and LSU to form a monosome. NSUN4 is thus a dual function protein, which on the one hand is needed for 12S rRNA methylation and, on the other hand interacts with MTERF4 to facilitate monosome assembly. The presented data suggest that NSUN4 has a key role in controlling a final step in ribosome biogenesis to ensure that only the mature SSU and LSU are assembled.
Environmental and Experimental Botany • Si nutrition is central mitigating abiotic and biotic stress in rice • Structural Si maintains yield through shoot strength and defends the plant from insect attack • Structural Si protects against, UV, water-stress, Na, Fe, Mn and Al toxicity and lodging • Si competes with As for uptake and Cd is bound to Si both in cell walls and phytoliths • Recycling straw phytolith Si is central to sustainable rice farming Abstract _____________________________________________________________________________________________ Adequate silicon fertilization greatly boosts rice yield and mitigates biotic and abiotic stress, and improves grain quality through lowering the content of cadmium and inorganic arsenic. This review on silicon dynamics in rice considers recent advances in our understanding of the role of silicon in rice, and the challenges of maintaining adequate silicon fertility within rice paddy systems. Silicon is increasingly considered as an element required for optimal plant performance, particularly in rice. Plants can survive with very low silicon under laboratory/glasshouse conditions, but this is highly artificial and, thus, silicon can be considered as essential for proper plant function in its environment. Silicon is incorporated into structural components of rice cell walls were it increases cell and tissue rigidity in the plant. Structural silicon provides physical protection to plants against microbial infection and insect attack as well as reducing the quality of the tissue to the predating organisms. The abiotic benefits are due to silicon's effect on overall organ strength. This helps protect against lodging, drought stress, high temperature (through efficient maintenance of transpiration), and photosynthesis by protecting against high UV. Furthermore, silicon also protects the plant from saline stress and against a range of toxic metal stresses (arsenic, cadmium, chromium, copper, nickel and zinc). Added to this, silicon application decreases grain concentrations of various human carcinogens, in particular arsenic, antimony and cadmium. As rice is efficient at stripping bioavailable silicon from the soil, recycling of silicon rich
Mitochondrial transcription termination factor 1, MTERF1, has been reported to couple rRNA gene transcription initiation with termination and is therefore thought to be a key regulator of mammalian mitochondrial ribosome biogenesis. The prevailing model is based on a series of observations published over the last two decades, but no in vivo evidence exists to show that MTERF1 regulates transcription of the heavy-strand region of mtDNA containing the rRNA genes. Here, we demonstrate that knockout of Mterf1 in mice has no effect on mitochondrial rRNA levels or mitochondrial translation. Instead, loss of Mterf1 influences transcription initiation at the light-strand promoter, resulting in a decrease of de novo transcription manifested as reduced 7S RNA levels. Based on these observations, we suggest that MTERF1 does not regulate heavy-strand transcription, but rather acts to block transcription on the opposite strand of mtDNA to prevent transcription interference at the light-strand promoter.
Significance Strigolactones are a new class of plant hormones regulating plant shoot and root architecture in response to the environment. Also present in root exudates, strigolactones stimulate the germination of parasitic plant seeds. This report describes a genomic polymorphism—associated with the Indica / Japonica subspecies divide in rice that has a major impact on the biosynthesis of strigolactones, plant tillering, and germination of the parasitic plant Striga hermonthica —consisting of the deletion of two strigolactone biosynthetic genes orthologous to Arabidopsis MAX1 . Both of these genes rescued the Arabidopsis max1-1 highly branched mutant phenotype and increased the strigolactone level when overexpressed in the Indica rice variety Bala. This finding is of great interest for plant physiologists, plant evolutionary biologists, and breeders.
Dietary restriction (DR) extends lifespan in a wide variety of species, yet the underlying mechanisms are not well understood. Here we show that the Caenorhabditis elegans HNF4α-related nuclear hormone receptor NHR-62 is required for metabolic and physiologic responses associated with DR-induced longevity. nhr-62 mediates the longevity of eat-2 mutants, a genetic mimetic of dietary restriction, and blunts the longevity response of DR induced by bacterial food dilution at low nutrient levels. Metabolic changes associated with DR, including decreased Oil Red O staining, decreased triglyceride levels, and increased autophagy are partly reversed by mutation of nhr-62. Additionally, the DR fatty acid profile is altered in nhr-62 mutants. Expression profiles reveal that several hundred genes induced by DR depend on the activity of NHR-62, including a putative lipase required for the DR response. This study provides critical evidence of nuclear hormone receptor regulation of the DR longevity response, suggesting hormonal and metabolic control of life span.
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