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Background Archaea form a third domain of life that is distinct from Bacteria and Eukarya. So far, many scholars have elucidated considerable details about the typical promoter architectures of the three domains of life. However, a functional promoter from the archaeon Halobacterium salinarum has never been studied in Escherichia coli. Results This paper found that the promoter of Halobacterium salinarum showed a promoter function in Escherichia coli. This Escherichia coli promoter structure contains − 10 box, -10 box extension and − 29 elements, however, no -35 box. The − 29 element is exercised by the TATA box in archaea. And we isolated the RM10 fragment that possessed the fusion characteristics of bacteria and archaea, which was overlapped with functionality of TATA box and − 29 elements. Conclusions The − 29 element reflects the evolutionary relationship between the archaeal promoter and the bacterial promoter. The result possibly indicated that there may be a certain internal connection between archaea and bacteria. We hypothesized that it provided a new viewpoint of the evolutionary relationship of archaea and other organisms.

Heterochromatin Protein 1 (HP1) is a conserved chromosomal protein in eukaryotic cells that has a major role in directing heterochromatin formation, a process that requires co-transcriptional gene silencing mediated by small RNAs and their associated argonaute proteins. Heterochromatin formation requires erasing the active epigenetic mark, such as H3K4me2, but the molecular link between HP1 and H3K4 demethylation remains unclear. In a fertility screen in female Drosophila, we identified ovaries absent (ova), which functions in the stem cell niche, downstream of Piwi, to support germline stem cell differentiation. Moreover, ova acts as a suppressor of position effect variegation, and is required for silencing telomeric transposons in the germline. Biochemically, Ova acts to link the H3K4 demethylase dLsd1 to HP1a for local histone modifications. Therefore, our study provides a molecular connection between HP1a and local H3K4 demethylation during HP1a-mediated gene silencing that is required for ovary development, transposon silencing, and heterochromatin formation. Editorial note: This article has been through an editorial process in which the authors decide how to respond to the issues raised during peer review. The Reviewing Editor's assessment is that all the issues have been addressed (see decision letter)., eLife digest The complete set of genetic material within a cell is known as a genome. The genomes of human and other animal cells have regions of active genes interspersed with ‘dark’ regions known as heterochromatin, which contain genes and other types of genetic material that have been inactivated. Heterochromatin commonly contains sections of genetic material known as transposons. When a transposon is active it is able to move around the genome, therefore, inactivating (or ‘silencing’) transposons helps to maintain the integrity of the genetic material in a cell. It is particularly important to silence transposons in the stem cells that produce sperm and egg cells – known as germline stem cells – to ensure genetic information is faithfully passed on to the next generation. A protein called HP1a plays a major role in directing where heterochromatin forms in the genome. This process requires an enzyme called dLsd1 to remove a small tag from the genetic material but it is not clear how HP1a regulates the activity of dLsd1. To address this question, Yang et al. studied how egg cells form in fruit flies, which are often used as models of animal biology in experiments. The team screened a population of fruit flies that carried mutations in many different genes to identify genes that affect the fertility of female flies. This revealed a gene named as ovaries absent (or ova for short) is required for egg cells to form. In germline stem cells ova silences transposons and in the surrounding tissue it represses a specific signal that usually maintains stem cells to allow the stem cells to divide to make egg cells. Further experiments using biochemical techniques found that the protein encoded by ova acts as a bridge to bring HP1a and dLsd1 together to silence genes in heterochromatin. The next step would be to identify the functional counterpart of the ova gene in mammals, including humans, which may help to discover causes of infertility and develop new fertility treatment.

Tubular sclerosis complex gene products TSC1 and TSC2 have evolutionarily conserved roles in cell growth from Drosophila to mammals. Here we reveal important roles for TSC1/2 in regulating intestinal stem cell (ISC) maintenance and differentiation of the enteroendocrine cell lineage in the Drosophila midgut. Loss of either the Tsc1 or Tsc2 gene in ISCs causes rapid ISC loss through TORC1 hyperactivation, because ISCs can be efficiently rescued by mutation of S6k or by rapamycin treatment. In addition, overexpression of Rheb, which triggers TORC1 activation, recapitulates the phenotype caused by TSC1/2 disruption. Genetic studies suggest that TSC1/2 maintains ISCs independently of nutritional status or Notch regulation, probably by inhibiting cell delamination. We show that Tsc1/Tsc2 mutant ISCs can efficiently produce enterocytes but not enteroendocrine cells, and this altered differentiation potential is also caused by hyperactivation of TORC1. Reduced TORC1-S6K signaling by mutation of S6k, however, has no effect on ISC maintenance or cell lineage differentiation. Our studies demonstrate that hyperactivation of TORC1 following the loss of TSC1/2 is detrimental to stem cell maintenance and multiple lineage differentiation in the Drosophila ISC lineage, a mechanism that could be conserved in other stem cell lineages, including that in humans.

Tuberous sclerosis complex human disease gene products TSC1 and TSC2 form a functional complex that negatively regulates target of rapamycin (TOR), an evolutionarily conserved kinase that plays a central role in cell growth and metabolism. Here, we describe a novel role of TSC1/2 in controlling stem cell maintenance. We show that in the Drosophila ovary, disruption of either the Tsc1 or Tsc2 gene in germline stem cells (GSCs) leads to precocious GSC differentiation and loss. The GSC loss can be rescued by treatment with TORC1 inhibitor rapamycin, or by eliminating S6K, a TORC1 downstream effecter, suggesting that precocious differentiation of Tsc1/2 mutant GSC is due to hyperactivation of TORC1. One well-studied mechanism for GSC maintenance is that BMP signals from the niche directly repress the expression of a differentiation-promoting gene bag of marbles (bam) in GSCs. In Tsc1/2 mutant GSCs, BMP signalling activity is downregulated, but bam expression is still repressed. Moreover, Tsc1 bam double mutant GSCs could differentiate into early cystocytes, suggesting that TSC1/2 controls GSC differentiation via both BMP-Bam-dependent and -independent pathways. Taken together, these results suggest that TSC prevents precocious GSC differentiation by inhibiting TORC1 activity and subsequently differentiation-promoting programs. As TSC1/2-TORC1 signalling is highly conserved from Drosophila to mammals, it could have a similar role in controlling stem cell behaviour in mammals, including humans.

Adenomatous polyposis coli (APC) and K-ras are the two most frequently mutated genes found in human colorectal cancers. In human colorectal cancers, Wnt signaling activation after the loss of APC is hypothesized to be the key event for adenoma initiation, whereas additional mutations such as Ras activation are required for the progression from adenoma to carcinoma. However, accumulating data have led to conflicting views regarding the precise role of Ras in APC loss-induced tumorigenesis. Here, using Drosophila midgut as a model system, we show that in the absence of Ras, APC mutant epithelial cells cannot initiate hyperplasia, suggesting that Ras plays an essential role in tumor initiation. Conversely, activating Ras by expressing oncogenic Ras or Raf in APC-deficient cells led to a blockage of cell differentiation and to preinvasive tumor outgrowth, characteristics that are shared by advanced colorectal carcinoma in humans. Mechanistically, we find that Ras is not required for Wnt signaling activation after APC loss, although Ras hyperactivation is able to potentiate Wnt signaling by increasing the cytoplasmic and nuclear accumulation of Armadillo/β-catenin via mechanisms independent of JNK/Rac1 or PI3K-Akt signaling, partly owing to the downregulation of DE-cadherin. Together with the data from gene expression analyses, our results indicate that both parallel and cooperative mechanisms of Wnt and Ras signaling are responsible for the initiation and progression of intestinal tumorigenesis after APC loss.