Near-infrared observations of active asteroid (3200) Phaethon reveal no evidence for hydration

Asteroid (3200) Phaethon is an active near-Earth asteroid and the parent body of the Geminid Meteor Shower. Because of its small perihelion distance, Phaethon's surface reaches temperatures sufficient to destabilize hydrated materials. We conducted rotationally resolved spectroscopic observations of this asteroid, mostly covering the northern hemisphere and the equatorial region, beyond 2.5-micron to search for evidence of hydration on its surface. Here we show that the observed part of Phaethon does not exhibit the 3-micron hydrated mineral absorption (within 2-sigma). These observations suggest that Phaethon's modern activity is not due to volatile sublimation or devolatilization of phyllosilicates on its surface. It is possible that the observed part of Phaethon was originally hydrated and has since lost volatiles from its surface via dehydration, supporting its connection to the Pallas family, or it was formed from anhydrous material

The operational environment and rotational acceleration of asteroid (101955) Bennu from OSIRIS-REx observations

During its approach to asteroid (101955) Bennu, NASA's Origins, Spectral Interpretation, Resource Identification, and Security-Regolith Explorer (OSIRIS-REx) spacecraft surveyed Bennu's immediate environment, photometric properties, and rotation state. Discovery of a dusty environment, a natural satellite, or unexpected asteroid characteristics would have had consequences for the mission's safety and observation strategy. Here we show that spacecraft observations during this period were highly sensitive to satellites (sub-meter scale) but reveal none, although later navigational images indicate that further investigation is needed. We constrain average dust production in September 2018 from Bennu's surface to an upper limit of 150 g s(-1) averaged over 34 min. Bennu's disk-integrated photometric phase function validates measurements from the pre-encounter astronomical campaign. We demonstrate that Bennu's rotation rate is accelerating continuously at 3.63 +/- 0.52 x 10(-6) degrees day(-2), likely due to the Yarkovsky-O'Keefe-Radzievskii-Paddack (YORP) effect, with evolutionary implications.This material is based upon work supported by NASA under Contract NNM10AA11C issued through the New Frontiers Program. This work made use of sbpy (http://sbpy. org), a community-driven Python package for small-body planetary astronomy supported by NASA PDART Grant No. 80NSSC18K0987. A portion of this research was carried out at the Jet Propulsion Laboratory, California Institute of Technology, under a contract with the National Aeronautics and Space Administration. M.A.B. and S.F. acknowledge financial support from CNES

29P/Schwassmann-Wachmann: A Rosetta Stone for Amorphous Water Ice and CO <-> CO2 Conversion in Centaurs and Comets?

Centaur 29P/Schwassmann-Wachmann 1 (SW1) is a highly active object orbiting in the transitional Gateway region (Sarid et al. 2019) between the Centaur and Jupiter Family Comet regions. SW1 is unique among the Centaurs in that it experiences quasi-regular major outbursts and produces CO emission continuously; however, the source of the CO is unclear. We argue that due to its very large size (approx. 32 km radius), SW1 is likely still responding, via amorphous water ice (AWI) conversion to crystalline water ice (CWI), to the rapid change in its external thermal environment produced by its dynamical migration from the Kuiper belt to the Gateway Region at the inner edge of the Centaur region at 6 au. It is this conversion process that is the source of the abundant CO and dust released from the object during its quiescent and outburst phases. If correct, these arguments have a number of important predictions testable via remote sensing and in situ spacecraft characterization, including: the quick release on Myr timescales of CO from AWI conversion for any few km-scale scattered disk KBO transiting into the inner system; that to date SW1 has only converted between 50 to 65% of its nuclear AWI to CWI; that volume changes upon AWI conversion could have caused subsidence and cave-ins, but not significant mass wasting or crater loss on SW1; that SW1s coma should contain abundant amounts of CWI CO2-rich icy dust particles; and that when SW1 transits into the inner system within the next 10,000 years, it will be a very different kind of JFC comet.Comment: 29 Pages, 3 Figures, 2 Tables, accepted 16-Sept-2022 by the Planetary Science Journal Corrected proof version 26-Oct-202

Inhibition of pluripotency networks by the Rb tumor suppressor restricts reprogramming and tumorigenesis

Mutations in the retinoblastoma tumor suppressor gene Rb are involved in many forms of human cancer. In this study, we investigated the early consequences of inactivating Rb in the context of cellular reprogramming. We found that Rb inactivation promotes the reprogramming of differentiated cells to a pluripotent state. Unexpectedly, this effect is cell cycle independent, and instead reflects direct binding of Rb to pluripotency genes, including Sox2 and Oct4, which leads to a repressed chromatin state. More broadly, this regulation of pluripotency networks and Sox2 in particular is critical for the initiation of tumors upon loss of Rb in mice. These studies therefore identify Rb as a global transcriptional repressor of pluripotency networks, providing a molecular basis for previous reports about its involvement in cell fate pliability, and implicate misregulation of pluripotency factors such as Sox2 in tumorigenesis related to loss of Rb function

Inhibition of pluripotency networks by the Rb tumor suppressor restricts reprogramming and tumorigenesis

Mutations in the retinoblastoma tumor suppressor gene Rb are involved in many forms of human cancer. In this study, we investigated the early consequences of inactivating Rb in the context of cellular reprogramming. We found that Rb inactivation promotes the reprogramming of differentiated cells to a pluripotent state. Unexpectedly, this effect is cell cycle independent, and instead reflects direct binding of Rb to pluripotency genes, including Sox2 and Oct4, which leads to a repressed chromatin state. More broadly, this regulation of pluripotency networks and Sox2 in particular is critical for the initiation of tumors upon loss of Rb in mice. These studies therefore identify Rb as a global transcriptional repressor of pluripotency networks, providing a molecular basis for previous reports about its involvement in cell fate pliability, and implicate misregulation of pluripotency factors such as Sox2 in tumorigenesis related to loss of Rb function

Myt1l safeguards neuronal identity by actively repressing many non-neuronal fates

Normal differentiation and induced reprogramming require the activation of target cell programs and silencing of donor cell programs(1,2). In reprogramming, the same factors are often used to reprogram many different donor cell types3. As most developmental repressors, such as RE1-silencing transcription factor (REST) and Groucho (also known as TLE), are considered lineage-specific repressors(4,5), it remains unclear how identical combinations of transcription factors can silence so many different donor programs. Distinct lineage repressors would have to be induced in different donor cell types. Here, by studying the reprogramming of mouse fibroblasts to neurons, we found that the pan neuron-specific transcription factor Myt1-like (Myt1l)(6) exerts its pro-neuronal function by direct repression of many different somatic lineage programs except the neuronal program. The repressive function of Myt1l is mediated via recruitment of a complex containing Sin3b by binding to a previously uncharacterized N-terminal domain. In agreement with its repressive function, the genomic binding sites of Myt1l are similar in neurons and fibroblasts and are preferentially in an open chromatin configuration. The Notch signalling pathway is repressed by Myt1l through silencing of several members, including Hes1. Acute knockdown of Myt1l in the developing mouse brain mimicked a Notch gain-of-function phenotype, suggesting that Myt1l allows newborn neurons to escape Notch activation during normal development. Depletion of Myt1l in primary postmitotic neurons de-repressed non-neuronal programs and impaired neuronal gene expression and function, indicating that many somatic lineage programs are actively and persistently repressed by Myt1l to maintain neuronal identity. It is now tempting to speculate that similar 'many-but-one' lineage repressors exist for other cell fates; such repressors, in combination with lineage-specific activators, would be prime candidates for use in reprogramming additional cell types.Non peer reviewe

DNMT3L Modulates Significant and Distinct Flanking Sequence Preference for DNA Methylation by DNMT3A and DNMT3B In Vivo

The DNTM3A and DNMT3B de novo DNA methyltransferases (DNMTs) are responsible for setting genomic DNA methylation patterns, a key layer of epigenetic information. Here, using an in vivo episomal methylation assay and extensive bisulfite methylation sequencing, we show that human DNMT3A and DNMT3B possess significant and distinct flanking sequence preferences for target CpG sites. Selection for high or low efficiency sites is mediated by the base composition at the −2 and +2 positions flanking the CpG site for DNMT3A, and at the −1 and +1 positions for DNMT3B. This intrinsic preference reproducibly leads to the formation of specific de novo methylation patterns characterized by up to 34-fold variations in the efficiency of DNA methylation at individual sites. Furthermore, analysis of the distribution of signature methylation hotspot and coldspot motifs suggests that DNMT flanking sequence preference has contributed to shaping the composition of CpG islands in the human genome. Our results also show that the DNMT3L stimulatory factor modulates the formation of de novo methylation patterns in two ways. First, DNMT3L selectively focuses the DNA methylation machinery on properly chromatinized DNA templates. Second, DNMT3L attenuates the impact of the intrinsic DNMT flanking sequence preference by providing a much greater boost to the methylation of poorly methylated sites, thus promoting the formation of broader and more uniform methylation patterns. This study offers insights into the manner by which DNA methylation patterns are deposited and reveals a new level of interplay between members of the de novo DNMT family

Photometry of Particles Ejected From Active Asteroid (101955) Bennu

AbstractNear‐Earth asteroid (101955) Bennu is an active asteroid experiencing mass loss in the form of ejection events emitting up to hundreds of millimeter‐ to centimeter‐scale particles. The close proximity of the Origins, Spectral Interpretations, Resource Identification, and Security–Regolith Explorer spacecraft enabled monitoring of particles for a 10‐month period encompassing Bennu's perihelion and aphelion. We found 18 multiparticle ejection events, with masses ranging from near zero to hundreds of grams (or thousands with uncertainties) and translational kinetic energies ranging from near zero to tens of millijoules (or hundreds with uncertainties). We estimate that Bennu ejects ~104 g per orbit. The largest event took place on 6 January 2019 and consisted of ~200 particles. The observed mass and translational kinetic energy of the event were between 459 and 528 g and 62 and 77 mJ, respectively. Hundreds of particles not associated with the multiparticle ejections were also observed. Photometry of the best‐observed particles, measured at phase angles between ~70° and 120°, was used to derive a linear phase coefficient of 0.013 ± 0.005 magnitudes per degree of phase angle. Ground‐based data back to 1999 show no evidence of past activity for Bennu; however, the currently observed activity is orders of magnitude lower than observed at other active asteroids and too low be observed remotely. There appears to be a gentle decrease in activity with distance from the Sun, suggestive of ejection processes such as meteoroid impacts and thermal fracturing, although observational bias may be a factor

The Oncoprotein EVI1 and the DNA Methyltransferase Dnmt3 Co-Operate in Binding and De Novo Methylation of Target DNA

EVI1 has pleiotropic functions during murine embryogenesis and its targeted disruption leads to prenatal death by severely affecting the development of virtually all embryonic organs. However, its functions in adult tissues are still unclear. When inappropriately expressed, EVI1 becomes one of the most aggressive oncogenes associated with human hematopoietic and solid cancers. The mechanisms by which EVI1 transforms normal cells are unknown, but we showed recently that EVI1 indirectly upregulates self-renewal and cell-cycling genes by inappropriate methylation of CpG dinucleotides in the regulatory regions of microRNA-124-3 (miR-124-3), leading to the repression of this small gene that controls normal differentiation and cell cycling of somatic cells. We used the regulatory regions of miR-124-3 as a read-out system to investigate how EVI1 induces de novo methylation of DNA. Here we show that EVI1 physically interacts with DNA methyltransferases 3a and 3b (Dnmt3a/b), which are the only de novo DNA methyltransferases identified to date in mouse and man, and that it forms an enzymatically active protein complex that induces de novo DNA methylation in vitro. This protein complex targets and binds to a precise region of miR-124-3 that is necessary for repression of a reporter gene by EVI1. Based on our findings, we propose that in cooperation with Dnmt3a/b EVI1 regulates the methylation of DNA as a sequence-specific mediator of de novo DNA methylation and that inappropriate EVI1 expression contributes to carcinogenesis through improper DNA methylation