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SUMMARY: Salt glands are the unique epidermal structures present in recretohalophytes, plants that actively excrete excess Na+ by salt secretory structures to avoid salt damage. Here, we describe a transmembrane protein that localizes to the plasma membrane of the recretohalophyte Limonium bicolor. As virus‐induced gene silencing of the corresponding gene LbRSG in L. bicolor decreased the number of salt glands, we named the gene Reduced Salt Gland. We detected LbRSG transcripts in salt glands by in situ hybridization and transient transformation. Overexpression and silencing of LbRSG in L. bicolor pointed to a positive role in salt gland development and salt secretion by interacting with Lb3G16832. Heterologous LbRSG expression in Arabidopsis enhanced salt tolerance during germination and the seedling stage by alleviating NaCl‐induced ion stress and osmotic stress after replacing or deleting the (highly) negatively charged region of extramembranous loop. After screened by immunoprecipitation‐mass spectrometry and verified using yeast two‐hybrid, PGK1 and BGLU18 were proposed to interact with LbRSG to strengthen salt tolerance. Therefore, we identified (highly) negatively charged regions in the extramembrane loop that may play an essential role in salt tolerance, offering hints about LbRSG function and its potential to confer salt resistance. Significance Statement: LbRSG (Reduced Salt Gland) was characterized as a transmembrane protein participating in salt gland development and salt resistance of recretohalophyte Limonium bicolor by interacting with Lb3G16832, and the negatively charged regions in the extramembranous loop were verified to play an essential role in salt tolerance of transgenic Arabidopsis. This study facilitated research on the molecular mechanisms of salt gland development and the design of salt‐tolerant crops for agricultural production in saline soils. [ABSTRACT FROM AUTHOR]

Halophytes complete their life cycles in saline environments. The recretohalophyte Limonium bicolor has evolved a specialized salt secretory structure, the salt gland, which excretes Na+ to avoid salt damage. Typical L. bicolor salt glands consist of 16 cells with four fluorescent foci and four secretory pores. Here, we describe a special type of salt gland at the base of the L. bicolor leaf petiole named bracelet salt glands due to their beaded‐bracelet‐like shape of blue auto‐fluorescence. Bracelet salt glands contain more than 16 cells and more than four secretory pores. Leaf disc secretion measurements and non‐invasive micro‐test techniques indicated that bracelet salt glands secrete more salt than normal salt glands, which helps maintain low Na+ levels at the leaf blade to protect the leaf. Cytokinin treatment induced bracelet salt gland differentiation, and the developed ones showed no further differentiation when traced with a living fluorescence microscopy imager, even though new salt gland development and leaf expansion were observed. Transcriptome revealed a NAC transcription factor gene that participates in bracelet salt gland development, as confirmed by its genome editing and overexpression in L. bicolor. These findings shed light on bracelet salt gland development and may facilitate the engineering of salt‐tolerant crops. [ABSTRACT FROM AUTHOR]

Phosphoglycerate dehydrogenase (PHGDH) is a key serine biosynthesis enzyme whose aberrant expression promotes various types of tumors. Recently, PHGDH has been found to have some non‐canonical functions beyond serine biosynthesis, but its specific mechanisms in tumorigenesis remain unclear. Here, we show that PHGDH localizes to the inner mitochondrial membrane and promotes the translation of mitochondrial DNA (mtDNA)‐encoded proteins in liver cancer cells. Mechanistically, we demonstrate that mitochondrial PHGDH directly interacts with adenine nucleotide translocase 2 (ANT2) and then recruits mitochondrial elongation factor G2 (mtEFG2) to promote mitochondrial ribosome recycling efficiency, thereby promoting mtDNA‐encoded protein expression and subsequent mitochondrial respiration. Moreover, we show that treatment with a mitochondrial translation inhibitor or depletion of mtEFG2 diminishes PHGDH‐mediated tumor growth. Collectively, our findings uncover a previously unappreciated function of PHGDH in tumorigenesis acting via promotion of mitochondrial translation and bioenergetics. Synopsis: This study reports a non‐catalytic tumorigenic role for serine biosynthesis enzyme phosphoglycerate dehydrogenase (PHGDH) in enhancing mitochondrial translation and respiratory metabolism in cancer cells, suggesting a new target for tumour progression. PHGDH localizes to the inner mitochondrial membrane in human liver cancer cells and patient tissues.PHGDH promotes translation of mtDNA‐encoded ETC proteins in catalytic activity‐independent manner.PHGDH forms a complex with mitochondrial translation factors ANT2 and mtEFG2, enhancing mtRRF interaction and mitoribosome recycling.PHGDH increases tumour growth in mice translation‐dependently by elevating respiratory metabolism. [ABSTRACT FROM AUTHOR]

Summary: Reduced substrates produced by the serpentinization reaction under hydration of olivine may have fuelled biological processes on early Earth. To understand the adaptive strategies and carbon metabolism of the microbes in the serpentinizing ecosystems, we reconstructed 18 draft genomes representing dominant species of Omnitrophicaeota, Gammaproteobacteria and Methanobacteria from the Manleluag serpentinizing spring in Zambales, Philippines (hyperalkaline and rich in methane and hydrogen). Phylogenomics revealed that two genomes were affiliated with a candidate phylum NPL‐UPA2 and the references of all our genomes were derived from ground waters, hot springs and the deep biosphere. C1 metabolism appears to be widespread as most of the genomes code for methanogenesis, CO oxidation and CO2 fixation. However, likely due to the low CO2 concentration and election acceptors, the biomass in the spring was extremely low (<103 cell/ml). Various Na+ and K+ transporters and Na+‐driving ATPases appear to be encoded by these genomes, suggesting that nutrient acquisition, bioenergetics and normal cytoplasmic pH were dependent on Na+ and K+ pumps. Our results advance our understanding of the metabolic potentials and bioenergetics of serpentinizing springs and provide a framework of the ecology of early Earth. [ABSTRACT FROM AUTHOR]

Summary: Large amounts of detrital organic matter and osmolytes accumulate in the sediments of hadal trenches (>6000 m depth) due to the funnelling effect. It is still unknown whether there are novel active microbes that depend on specific carbon sources in extreme and isolated environments. In this study, we present a novel active bacterial phylum, Candidatus Tianyabacteria in the FCB superphylum, which was enriched in sediments collected from the Challenger Deep. Genome binning resulted in high‐quality Ca. Tianyabacteria genomes representing two Ca. Tianyabacteria lineages (L1 and L2) in sediments 0–21 cm below the surface (cmbsf); L1 tends to be abundant in the upper layers (0–9 cmbsf), and L2 seems to be more prevalent in the deeper layers (12–21 cmbsf). Gene annotation and transcriptomics results indicate that the two lineages might import and catalyse amino acids and myo‐inositol into central carbon metabolism for a heterotrophic lifestyle. Probably due to differences in environmental oxygen levels, the L2 genomes harbour gene clusters responsible for denitrification and fermentation, while the L1 genomes encode octahaem cytochrome c and multicopper oxidase using unknown substrates. The Ca. Tianyabacteria are thus novel heterotrophic organisms that participate in processes of carbon, nitrogen and organic osmolyte cycling in hadal sediments. [ABSTRACT FROM AUTHOR]

The MYC oncoprotein activates and represses gene expression in a transcription‐dependent or transcription‐independent manner. Modification of mRNA emerges as a key gene expression regulatory nexus. We sought to determine whether MYC alters mRNA modifications and report here that MYC promotes cancer progression by down‐regulating N6‐methyladenosine (m6A) preferentially in transcripts of a subset of MYC‐repressed genes (MRGs). We find that MYC activates the expression of ALKBH5 and reduces m6A levels in the mRNA of the selected MRGs SPI1 and PHF12. We also show that MYC‐regulated m6A controls the translation of MRG mRNA via the specific m6A reader YTHDF3. Finally, we find that inhibition of ALKBH5, or overexpression of SPI1 or PHF12, effectively suppresses the growth of MYC‐deregulated B‐cell lymphomas, both in vitro and in vivo. Our findings uncover a novel mechanism by which MYC suppresses gene expression by altering m6A modifications in selected MRG transcripts promotes cancer progression. SYNOPSIS: MYC suppresses gene expression by indirectly altering m6A modifications in transcripts of MYC‐repressed genes via ALKBH5 to promote cancer progression. MYC indirectly down‐regulates m6A levels in mRNA and inhibits protein expression of selected MRG transcripts.MYC transcriptionally activates the m6A demethylases ALKBH5 and FTO.ALKBH5 removes m6A and YTHDF3 binds m6A‐modified mRNAs to regulate the translation of SPI1/PHF12.The MYC‐ALKBH5‐m6A‐SPI1/PHF12 axis is critical for cancer progression. [ABSTRACT FROM AUTHOR]