Ras promotes cell survival by antagonizing both JNK and Hid signals in the Drosophila eye

<p>Abstract</p> <p>Background</p> <p>Programmed cell death, or apoptosis, is a fundamental physiological process during normal development or in pathological conditions. The activation of apoptosis can be elicited by numerous signalling pathways. Ras is known to mediate anti-apoptotic signals by inhibiting Hid activity in the <it>Drosophila </it>eye. Here we report the isolation of a new loss-of-function <it>ras </it>allele, <it>ras</it>^<it>KP</it>, which causes excessive apoptosis in the <it>Drosophila </it>eye.</p> <p>Results</p> <p>This new function is likely to be mediated through the JNK pathway since the inhibition of JNK signalling can significantly suppress <it>ras</it>^<it>KP</it>-induced apoptosis, whereas the removal of <it>hid </it>only weakly suppresses the phenotype. Furthermore, the reduction of JNK signalling together with the expression of the baculovirus caspase inhibitor p35, which blocks Hid activity, strongly suppresses the <it>ras</it>^{<it>KP </it>}cell death. In addition, we find a strong correlation between <it>ras</it>^<it>KP</it>-induced apoptosis in the eye disc and the activation of JNK signalling.</p> <p>Conclusion</p> <p>In the <it>Drosophila </it>eye, Ras may protect cells from apoptosis by inhibiting both JNK and Hid activities. Surprisingly, reducing Ras activity in the wing, however, does not cause apoptosis but rather affects cell and organ size. Thus, in addition to its requirement for cell viability, Ras appears to mediate different biological roles depending on the developmental context and on the level of its expression.</p

A reference-grade wild soybean genome

Wild relatives of crop plants are invaluable germplasm for genetic improvement. Here, Xie et al. report a reference-grade wild soybean genome and show that it can be used to identify structural variation and refine quantitative trait loci

A reference-grade wild soybean genome

Efficient crop improvement depends on the application of accurate genetic information contained in diverse germplasm resources. Here we report a reference-grade genome of wild soybean accession W05, with a final assembled genome size of 1013.2 Mb and a contig N50 of 3.3 Mb. The analytical power of the W05 genome is demonstrated by several examples. First, we identify an inversion at the locus determining seed coat color during domestication. Second, a translocation event between chromosomes 11 and 13 of some genotypes is shown to interfere with the assignment of QTLs. Third, we find a region containing copy number variations of the Kunitz trypsin inhibitor (KTI) genes. Such findings illustrate the power of this assembly in the analysis of large structural variations in soybean germplasm collections. The wild soybean genome assembly has wide applications in comparative genomic and evolutionary studies, as well as in crop breeding and improvement programs

Mst1 and mst2 are essential regulators of trophoblast differentiation and placenta morphogenesis.

The placenta is essential for survival and growth of the fetus because it promotes the delivery of nutrients and oxygen from the maternal circulation as well as fetal waste disposal. Mst1 and Mst2 (Mst1/2), key components of the mammalian hpo/Mst signaling pathway, encode two highly conserved Ser/Thr kinases and play important roles in the prevention of tumorigenesis and autoimmunity, control of T cell development and trafficking, and embryonic development. However, their functions in placental development are not fully understood, and the underlying cellular and molecular mechanisms remain elusive. Here, we investigated the functions of Mst1/2 in mouse placental development using both conventional and conditional (endothelial) Mst1/2 double knockout mice. We found that the number of trophoblast giant cells dramatically increased while spongiotrophoblast cells almost completely disappeared in Mst1/2 deficient placentas. We showed that Mst1/2 deficiency down regulated the expression of Mash2, which is required for suppressing the differentiation of trophoblast giant cells. Furthermore, we demonstrated that endothelial-specific deletion of Mst1/2 led to impaired placental labyrinthine vasculature and embryonic lethality at E11.5, but neither affected vasculature in yolk sac and embryo proper nor endocardium development. Collectively, our findings suggest that Mst1/2 regulate placental development by control of trophoblast cell differentiation and labyrinthine vasculature at midgestation and Mst1/2 control labyrinth morphogenesis in trophoblast- and fetal endothelial-dependent manners. Thus, our studies have defined novel roles of Mst1/2 in mouse placental development

Unveiling the Anomalous Hall Response of the Magnetic Structure Changes in the Epitaxial MnBi₂Te₄ Films

Recently discovered as an intrinsic antiferromagnetic topological insulator, MnBi2Te4 has attracted tremendous research interest, as it provides an ideal platform to explore the interplay between topological and magnetic orders. MnBi2Te4 displays distinct exotic topological phases that are inextricably linked to the different magnetic structures of the material. In this study, we conducted electrical transport measurements and systematically investigated the anomalous Hall response of epitaxial MnBi2Te4 films when subjected to an external magnetic field sweep, revealing the different magnetic structures stemming from the interplay of applied fields and the material’s intrinsic antiferromagnetic (AFM) ordering. Our results demonstrate that the nonsquare anomalous Hall loop is a consequence of the distinct reversal processes within individual septuple layers. These findings shed light on the intricate magnetic structures in MnBi2Te4 and related materials, offering insights into understanding their transport properties and facilitating the implementation of AFM topological electronics

Defective labyrinthine vascularization/morphogenesis in <i>Mst1/2</i> CKO placentas.

<p>(A) RT-PCR analysis of <i>Mst1/2</i> expression in the purified endothelial cells from E10.5 wild type embryos and yolk sacs (left panel) and Flow cytometry analysis of CD31 expression of the purified endothelial cells (right panel). (B) Images of X-gal-stained E9.5 placental cryosections with indicated genotypes. Note: <i>β-gal</i> gene was expressed on blood vessels containing nucleated fetal red blood cells. Black dashed lines indicate the spongiotrophoblast layer. (C) Images of whole-mount X-gal-stained E9.5 yolk sacs with indicated genotypes. (D and E) Images of HE-stained cryosections of Ctr and <i>Mst1/2 </i>CKO placentas at E9.5 (D) and E10.5 (E). High magnification images of the cropped region in (D) and (E) are shown under each panel, respectively. The white dashed lines are the boundaries between maternal decidua and trophoblast giant cell layer. Black dashed lines mark the spongiotrophoblast layer. (F) Statistical analysis of the percentage of fetal blood vessels and maternal sinusoids in the labyrinth layer of control and <i>Mst1/2</i> CKO placentas at E10.5. Data are expressed as the means ± SEM (three sections/placenta, three placentas from three pregnant mice per group, ** <i>P</i><0.01). (G) CD31 immunofluoresence staining of cryosections of E10.5 control and <i>Mst1/2 </i>CKO placentas. The labyrinth layer is defined by the red dashed lines. Arrows and arrowheads indicate fetal nucleated and maternal enucleated red blood cells, respectively. Images are representative sections from at least three placentas per group. Al, allantois; Ctr, control; De, decidua; Gi, trophoblast giant cells; Iso, Isotype control; La, labyrinth; Sp, spongiotrophoblast layer.</p

Numbers of <i>Mst1/2</i> CKO and Ctr offsprings.

<p>Cross: <i>Mst1</i>^+/fl;<i>Mst2</i>^−/−<i>;Tie2-Cre</i> X <i>Mst1</i>^fl/fl;<i>Mst2</i>^−/−.</p><p>Ctr includes: <i>Mst1^+/fl;Mst2^−/−;Tie2-Cre</i>, <i>Mst1^fl/fl;Mst2^−/−</i>, <i>Mst1^+/fl;Mst2^−/−</i>.</p><p>ND: not determined.</p><p>*dead embryos.</p