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Marrow stromal cells (MSCs, also termed mesenchymal stem cells) have been proposed as a promising cellular therapy for tissue injury including radiation-induced marrow failure, but evidence for a direct effect is lacking. To assess the effects of MSCs on survival after lethal irradiation, we infused syngeneic MSCs (either as immortalized MSCs clones or primary MSCs) intravenously into wild-type C57/Bl6 mice within 24 hours of lethal total body irradiation (TBI). Mice receiving either of the MSC preparations had significantly improved survival when compared to controls. In vivo imaging, immune histochemistry, and RT-PCR employed to detect MSCs indicated that the infused MSCs were predominantly localized to the lungs and rapidly cleared following infusion. Our results suggest that a single infusion of MSCs can improve survival after otherwise lethal TBI but the effect is not due to a direct interaction with, or contribution to, the damaged marrow by MSCs [ABSTRACT FROM AUTHOR]

Agriculture is an important component of the Indian Economy. It contributes to about 21% of India's Gross Domestic Product (GDP), 11% of total exports and provides employment to around 60% of the work force and is directly related to self-reliance, meeting the food and nutritional security of the people, equitable distribution of income and wealth in rural areas, reduction of poverty and improvement in the quality of life. The liberalized economic policies resulted in a commendable growth of some sectors of the economy, but when it comes to agricultural development, the growth scenario presents a dismal and bleak picture. There has been a consistent decline in the growth of the agricultural sector since 1990 compared to the 1980s. Commodity markets and warehouse financing are innovative initiatives devised specifically to revive and resurrect the agricultural sector with the twin objectives of providing price discovery and risk mitigation to the farmers. This article delves into all the relevant aspects of warehouse finance and warehouse infrastructure in India. [ABSTRACT FROM AUTHOR]

Abstract: This paper concerns the stability of anode-supported solid oxide fuel cells (SOFCs), operated with fuel mixtures of methane–CO2 and methane–air. Stability, which was evaluated in terms of voltage decrease at constant current density, was affected by coke deposits. Chemically inert anode barrier layers were shown to enhance stability and to slow catalytic endothermic reforming reactions within the Ni–YSZ anode that otherwise caused deleterious temperature variations and cell cracking. Increasing the amount of CO2 added to CH4 fuel led to a wider stable operating range, yet had relatively little effect on SOFC performance. Button cells operated at 800 C with fuel streams of 75% CH4 and 25% CO2 achieved maximum power densities above 1W/cm2. Adding air to methane also increased stability. In the case of air addition, SOFC temperature increased as a consequence of exothermic partial-oxidation reforming chemistry. Models were developed to predict temperature and gas-composition profiles within the button cells. The simulation results were used to assist interpretation of the experimental observations. [Copyright &y& Elsevier]

Abstract: Solid oxide fuel cells with Sr0.8La0.2TiO3 anode-side supports, Ni- Sm-doped ceria adhesion layer, Ni- Y2O3-stabilized ZrO2 (YSZ) anode active layer, YSZ electrolyte, and La0.8Sr0.2MnO3(LSM)–YSZ cathode are described. These cells are stable in simulated natural gas at current densities as low as 0.2Acm−2. This represents much-improved stability against coking in natural gas, compared with conventional Ni–YSZ anode-supported SOFCs which rapidly coke, even at higher current densities. Cell operation in H2 fuel with 50–100ppm, H2S results in an initial decrease in cell power density, but no long-term degradation occurs and full recovery to the initial performance level is observed after dry H2 fuel flow is restored. Degradation is not observed during or after seven redox cycles between H2 and air. [Copyright &y& Elsevier]

This article describes results on methane partial oxidation in (La0.6Sr0.4)(Ga0.8Mg0.05Co0.15)O3 ceramic membrane reactors. The thin membranes were fabricated by co-firing with porous composite NiO–La-doped Ceria (LDC) supports. A La0.6Sr0.4Fe0.2Co0.8O3-based composite layer on the air side of the membrane promoted fast oxygen reduction. Electrical measurements indicated that LSGMC showed good mixed conductivity and that oxygen transport was co-limited by bulk and interfacial processes. The O2 permeation rate during methane partial oxidation at 750 °C was ≈10–12 sccm/cm2, with a maximum syngas production rate of 60–70 sccm/cm2. [ABSTRACT FROM AUTHOR]

The article reports on India's compliance with trade-related aspects of intellectual property rights (TRIPS) and its effort to read further limitations into TRIPS as of 2005. It states that the Expert Committee can limit interpretation of TRIPS as against the Patents Act if it views the patentability exclusion of microorganisms and non-new chemical entity (NCE) product inventions will violate TRIPS provisions. Otherwise, amendments to the Patents Act will reportedly require more explanation.

This article comments on the passing of the Patents (Amendment) Act, 2005 and the TRIPS Agreement. It explores the controversial Section 5 of the Indian Patents Act that provided only limited term process patent protection for inventions relating to food, drug, and medicine. The provision enabled the development of a generic pharmaceutical industry in India.

The different parts of Momordica charantia have been reported to have several therapeutic applications against hyperglycemia and hypercholesterolemia associated with pancreatic lipase (PL). Inhibition of this enzyme prevents the absorption of dietary triglyceride in the intestine, and thus exerts an anti‐obesity effect. This study aimed to investigate the bioactive constituents of the fruits of M. charantia (MCF) extract and fractions against pancreatic PL followed by study of their inhibition kinetics. The PL inhibitory assay was performed spectrophotometrically by measuring the change in absorbance of the products at 405 nm, using p‐nitrophenylcaprylate as substrate. The results indicated that the ethyl acetate fraction of MCF (EFMC) offered significant, dose‐dependent inhibition against PL, compared with the positive control, Orlistat. The enzyme kinetics study revealed the inhibition to be a mixed type in nature. Additionally, the total phenol and flavonoid content of the fractions was estimated. A positive correlation between phenolic content of EFMC and its PL inhibitory activity was established statistically, which implied that higher inhibition potential was contributed by the phenolic compounds. The identification of the bioactive constituents was further confirmed by LC–QTOF–MS study. This finding suggested that phenolic compounds of MCF can serve as functional food components to address obesity‐related disorders linked with PL. [ABSTRACT FROM AUTHOR]

Members of Brassica seed oil are important sources of nutritionally superior edible oil. There are no comprehensive reports on complete lipidomic profile of these oilseed crops. In this study, the lipidomic profiling of edible oil from 7 different cultivated species of Brassica seed oils was performed by shotgun approach using electrospray High Resolution Time of Flight-Mass Spectrometry (ESI-ToF-MS). The mass spectrum under positive polarity revealed 1098 lipids under different lipid classes including sphingolipids, phospholipids and different storage lipids. Under negative polarity, 70 lipids including free fatty acids (FFA), cardiolipins and phospholipids were detected. Erucic acid in FFA form was found to be most abundant in both Yellow and Brown sarson. Brassica napus contains almost all forms of cardiolipins (CL). Out of 26 different species of cardiolipins detected in negative ion mode, CL 56:1 (FA 18:1) and CL 56:1 (FA 22:1) were present only in brown sarson. Similarly, CL 56:2 (FA 18:2) and CL 56:1 (FA 22:1) were present only in Yellow and Brown sarson. These findings enhance our understanding of the nutritional diversity in Brassica seed oils, emphasizing the significance of lipidomic analysis for elucidating the molecular composition of edible oils. [ABSTRACT FROM AUTHOR]

Scalable isogenic models of cancer-associated mutations are critical to studying dysregulated gene function. Nonsynonymous mutations of splicing factors, which typically affect one allele, are common in many cancers, but paradoxically confer growth disadvantage to cell lines, making their generation and expansion challenging. Here, we combine AAV-intron trap, CRISPR/Cas9, and inducible Cre-recombinase systems to achieve >90% efficiency to introduce the oncogenic K700E mutation in SF3B1, a splicing factor commonly mutated in multiple cancers. The intron-trap design of AAV vector limits editing to one allele. CRISPR/Cas9-induced double stranded DNA breaks direct homologous recombination to the desired genomic locus. Inducible Cre-recombinase allows for the expansion of cells prior to loxp excision and expression of the mutant allele. Importantly, AAV or CRISPR/Cas9 alone results in much lower editing efficiency and the edited cells do not expand due to toxicity of SF3B1-K700E. Our approach can be readily adapted to generate scalable isogenic systems where mutant oncogenes confer a growth disadvantage. Boddu et al combined AAV-intron trap, CRISPR/Cas9 and inducible Cre-recombinase systems to introduce the oncogenic K700E mutation in SF3B1, which is a splicing factor commonly mutated in multiple cancers, with more than 90% efficiency. Their approach can be readily adapted to generate scalable isogenic systems where mutant oncogenes are detrimental to cell culture growth. [ABSTRACT FROM AUTHOR]

Transcription and splicing of pre-messenger RNA are closely coordinated, but how this functional coupling is disrupted in human diseases remains unexplored. Using isogenic cell lines, patient samples, and a mutant mouse model, we investigated how cancer-associated mutations in SF3B1 alter transcription. We found that these mutations reduce the elongation rate of RNA polymerase II (RNAPII) along gene bodies and its density at promoters. The elongation defect results from disrupted pre-spliceosome assembly due to impaired protein-protein interactions of mutant SF3B1. The decreased promoter-proximal RNAPII density reduces both chromatin accessibility and H3K4me3 marks at promoters. Through an unbiased screen, we identified epigenetic factors in the Sin3/HDAC/H3K4me pathway, which, when modulated, reverse both transcription and chromatin changes. Our findings reveal how splicing factor mutant states behave functionally as epigenetic disorders through impaired transcription-related changes to the chromatin landscape. We also present a rationale for targeting the Sin3/HDAC complex as a therapeutic strategy. [Display omitted] • SF3B1 oncogenic mutations reduce RNAPII gene-body elongation rate and promoter density • RNAPII elongation defect is linked to disruption of the early spliceosome assembly • Chromatin landscape is altered, rendering these functionally epigenetic disorders • Sin3/HDAC pathway can be therapeutically targeted in SF3B1 mutant disease Boddu et al. reveal how common cancer-associated mutations in SF3B1, a core splicing factor, alter RNAPII transcription kinetics through impaired early spliceosome assembly. Transcription defects alter chromatin organization at gene promoters, which can be reversed by inhibiting the Sin3/HDAC complex, providing a potential therapeutic strategy. [ABSTRACT FROM AUTHOR]

Serine racemase (SR) converts the free form of L-serine into D-serine (DS) in the mammalian brain. The DS functions as a co-agonist of N-methyl D-aspartate (NMDA) receptor. The over- activation of NMDA receptor leads to many neurological disorders like stroke, amyotrophic lateral sclerosis, Alzheimer's disease and an effective inhibitor of SR could be a corrective method for the receptor over-activation. We report for the first time here a rapid way of purifying and identifying an inhibitor from medicinal plants known to have the neuro-protective effect. We have purified SR inhibitor from the methanolic extract of Centella asiatica by affinity method. High resolution mass spectrometry and infrared spectroscopy were used to identify the ligand to be madecassoside. We have shown the madecassoside binding in silico and its inhibition of recombinant human serine racemase in vitro and ex vivo. [ABSTRACT FROM AUTHOR]

The cohesin complex regulates sister chromatid cohesion, chromosome organization, gene expression, and DNA repair. Cohesin is a ring complex composed of four core subunits and seven regulatory subunits. In an effort to comprehensively identify additional cohesin-interacting proteins, we used gene editing to introduce a dual epitope tag into the endogenous allele of each of 11 known components of cohesin in cultured human cells, and we performed MS analyses on dual-affinity purifications. In addition to reciprocally identifying all known components of cohesin, we found that cohesin interacts with a panoply of splicing factors and RNA-binding proteins (RBPs). These included diverse components of the U4/U6.U5 tri-small nuclear ribonucleoprotein complex and several splicing factors that are commonly mutated in cancer. The interaction between cohesin and splicing factors/RBPs was RNA- and DNA-independent, occurred in chromatin, was enhanced during mitosis, and required RAD21. Furthermore, cohesin-interacting splicing factors and RBPs followed the cohesin cycle and prophase pathway of cell cycle-regulated interactions with chromatin. Depletion of cohesin-interacting splicing factors and RBPs resulted in aberrant mitotic progression. These results provide a comprehensive view of the endogenous human cohesin interactome and identify splicing factors and RBPs as functionally significant cohesin-interacting proteins. [ABSTRACT FROM AUTHOR]

Existing understanding of molecular composition of sputum and its role in tuberculosis patients is variously limited to its diagnostic potential. We sought to identify infection induced sputum proteome alteration in active/non tuberculosis patients (A/NTB) and their role in altered lung patho-physiology. Out of the study population (n = 118), sputum proteins isolated from discovery set samples (n = 20) was used for an 8-plex isobaric tag for relative and absolute concentration analysis. A minimum set of protein with at least log2(ATB/NTB) >±1.0 in ATB was selected as biosignature and validated in 32 samples. Predictive accuracy was calculated from area under the receiver operating characteristic curve (AUC of ROC) using a confirmatory set (n = 50) by Western blot analysis. Mass spectrometry analysis identified a set of 192 sputum proteins, out of which a signature of β-integrin, vitamin D binding protein:DBP, uteroglobin, profilin and cathelicidin antimicrobial peptide was sufficient to differentiate ATB from NTB. AUC of ROC of the biosignature was calculated to 0.75. A shift in DBP-antimicrobial peptide (AMP) axis in the lungs of tuberculosis patients is observed. The identified sputum protein signature is a promising panel to differentiate ATB from NTB groups and suggest a deregulated DBP-AMP axis in lungs of tuberculosis patients. [ABSTRACT FROM AUTHOR]

Acute myeloid leukemia (AML) presents a pressing medical need in that it is largely resistant to standard chemotherapy as well as modern therapeutics, such as targeted therapy and immunotherapy, including anti-programmed cell death protein (anti-PD) therapy. We demonstrate that programmed death-1 homolog (PD-1H), an immune coinhibitory molecule, is highly expressed in blasts from the bone marrow of AML patients, while normal myeloid cell subsets and T cells express PD-1H. In studies employing syngeneic and humanized AML mouse models, overexpression of PD-1H promoted the growth of AML cells, mainly by evading T cell-mediated immune responses. Importantly, ablation of AML cell-surface PD-1H by antibody blockade or genetic knockout significantly inhibited AML progression by promoting T cell activity. In addition, the genetic deletion of PD-1H from host normal myeloid cells inhibited AML progression, and the combination of PD-1H blockade with anti-PD therapy conferred a synergistic antileukemia effect. Our findings provide the basis for PD-1H as a potential therapeutic target for treating human AML.

Fanconi anemia (FA) is characterized by congenital abnormalities, bone marrow failure, and cancer susceptibility. The central FA protein complex FANCI/FANCD2 (ID2) is activated by monoubiquitination and recruits DNA repair proteins for interstrand crosslink (ICL) repair and replication fork protection. Defects in the FA pathway lead to R-loop accumulation, which contributes to genomic instability. Here, we report that the splicing factor SRSF1 and FANCD2 interact physically and act together to suppress R-loop formation via mRNA export regulation. We show that SRSF1 stimulates FANCD2 monoubiquitination in an RNA-dependent fashion. In turn, FANCD2 monoubiquitination proves crucial for the assembly of the SRSF1-NXF1 nuclear export complex and mRNA export. Importantly, several SRSF1 cancer-associated mutants fail to interact with FANCD2, leading to inefficient FANCD2 monoubiquitination, decreased mRNA export, and R-loop accumulation. We propose a model wherein SRSF1 and FANCD2 interaction links DNA damage response to the avoidance of pathogenic R-loops via regulation of mRNA export., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Mutations in the SF3B1 splicing factor are commonly seen in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML), yet the specific oncogenic pathways activated by mis-splicing have not been fully elucidated. Inflammatory immune pathways have been shown to play roles in the pathogenesis of MDS, though the exact mechanisms of their activation in splicing mutant cases are not well understood., Methods: RNA-seq data from SF3B1 mutant samples was analyzed and functional roles of interleukin-1 receptor-associated kinase 4 ( IRAK4) isoforms were determined. Efficacy of IRAK4 inhibition was evaluated in preclinical models of MDS/AML., Results: RNA-seq splicing analysis of SF3B1 mutant MDS samples revealed retention of full-length exon 6 of IRAK4 , a critical downstream mediator that links the Myddosome to inflammatory NF-kB activation. Exon 6 retention leads to a longer isoform, encoding a protein (IRAK4-long) that contains the entire death domain and kinase domain, leading to maximal activation of NF-kB. Cells with wild-type SF3B1 contain smaller IRAK4 isoforms that are targeted for proteasomal degradation. Expression of IRAK4-long in SF3B1 mutant cells induces TRAF6 activation leading to K63-linked ubiquitination of CDK2, associated with a block in hematopoietic differentiation. Inhibition of IRAK4 with CA-4948, leads to reduction in NF-kB activation, inflammatory cytokine production, enhanced myeloid differentiation in vitro and reduced leukemic growth in xenograft models., Conclusions: SF3B1 mutation leads to expression of a therapeutically targetable, longer, oncogenic IRAK4 isoform in AML/MDS models., Funding: This work was supported by Cincinnati Children's Hospital Research Foundation, Leukemia Lymphoma Society, and National Institute of Health (R35HL135787, RO1HL111103, RO1DK102759, RO1HL114582), Gabrielle's Angel Foundation for Cancer Research, and Edward P. Evans Foundation grants to DTS. AV is supported by Edward P. Evans Foundation, National Institute of Health (R01HL150832, R01HL139487, R01CA275007), Leukemia and Lymphoma Society, Curis and a gift from the Jane and Myles P. Dempsey family. AP and JB are supported by Blood Cancer UK (grants 13042 and 19004). GC is supported by a training grant from NYSTEM. We acknowledge support of this research from The Einstein Training Program in Stem Cell Research from the Empire State Stem Cell Fund through New York State Department of Health Contract C34874GG. MS is supported by a National Institute of Health Research Training and Career Development Grant (F31HL132420)., Competing Interests: GC, AP, BA, TB, SG, SS, SP, NS, SA, RA, SA, LS, VS, MC, KP, TB, MP, BW, AW, AS, EG, JB No competing interests declared, MS MS owns stock options in Poseida Therapeutics. The author has no other competing interests to declare, RB RB is a former employee of Curis, Inc, and holds patents patents related to CA-4948 (WO-2019089580-A1). RB also owns stocks in Curis, Inc. The author has no other competing interests to declare, MR MR is an employee of Aurigene Inc, MS MS owns stock options in Curis, Inc as an employee. The author has no other competing interests to declare, RB RKB is a named inventor on patent applications related to treating cancers with SF3B1 mutations filed by Fred Hutchinson Cancer Research Center (METHODS AND COMPOSITIONS COMPRISING BRD9 ACTIVATING THERAPIES FOR TREATING CANCERS AND RELATED DISORDERS - PCT/US2020/039645; SYNTHETIC INTRONS FOR TARGETED GENE EXPRESSION - PCT/US21/56273).The author has no other competing interests to declare, RM REM is an employee of Curis, Inc and has received honoria payments and also holds stocks in the company. The author has no other competing interests to declare, US US held grants from Bayer Healthcare and Aileron Therapauetics, and received consultancy fees from Aileron Therapeutics, Stelexis Therapeutics, Pieris Pharmaceuticals and Trillium Therapeutics. US is Director at Stelexis Therapeutics and holds stocks in the company. The author has no other competing interests to declare, DS DS received consultancy fees from Kurome Therapeutics, Treeline Biosciences, Tolero Therapeutics, and Captor Therapeutics. DS also owns stocks in Kurome Therapeutics. The author has no other competing interests to declare, AV AV has received research funding from GlaxoSmithKline, BMS, Jannsen, Incyte, MedPacto, Celgene, Novartis, Curis, Prelude and Eli Lilly and Company, has received compensation as a scientific advisor to Novartis, Stelexis Therapeutics, Acceleron Pharma, and Celgene, and has equity ownership in Throws Exception and Stelexis Therapeutics, (© 2022, Choudhary, Pellagatti et al.)

Lithium-ion batteries (LIBs) are the most preferred energy storage devices today for many high-performance applications. Recently, concerns about global warming and climate change have increased the need and requirements for LIBs used in electric vehicles, and thus more advanced technologies and materials are urgently needed. Among the anode materials under development, silicon (Si) has been considered the most promising anode candidate for the next generation LIBs to replace the widely used graphite. Si cannot be used as such as the electrode of LIB, and thus, carbon is commonly used to realize the applicability of Si in LIBs. Typically, this means forming a-Si/carbon composite (Si/C). One of the main challenges in the industrial development of high-performance LIBs is to exploit low-cost, environmentally benign, sustainable, and renewable chemicals and materials. In this regard, bio-based Si and carbon are favorable to address the challenge assuming that the performance of the LIB anode is not compromised. The present review paper focuses on the development of Si and carbon anodes derived from various types of biogenic sources, particularly from plant-derived biomass resources. An overview of the biomass precursors, process/extraction methods for producing Si and carbon, the critical physicochemical properties influencing the lithium storage in LIBs, and how they affect the electrochemical performance are highlighted. The review paper also discusses the current research challenges and prospects of biomass-derived materials in developing advanced battery materials., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Muraleedharan Pillai, Kalidas, Zhao and Lehto.)

Musashi 2 (MSI2) is an RNA binding protein (RBP) that regulates asymmetric cell division and cell fate decisions in normal and cancer stem cells. MSI2 appears to repress translation by binding to 3' untranslated regions (3'UTRs) of mRNA, but the identity of functional targets remains unknown. Here, we used individual nucleotide resolution cross-linking and immunoprecipitation (iCLIP) to identify direct RNA binding partners of MSI2 and integrated these data with polysome profiling to obtain insights into MSI2 function. iCLIP revealed specific MSI2 binding to thousands of mRNAs largely in 3'UTRs, but translational differences were restricted to a small fraction of these transcripts, indicating that MSI2 regulation is not triggered by simple binding. Instead, the functional targets identified here were bound at higher density and contain more 'UAG' motifs compared to targets bound nonproductively. To further distinguish direct and indirect targets, MSI2 was acutely depleted. Surprisingly, only 50 transcripts were found to undergo translational induction on acute loss. Using complementary approaches, we determined eukaryotic translation initiation factor 3A (EIF3A) to be an immediate, direct target. We propose that MSI2 downregulation of EIF3A amplifies these effects on translation. Our results also underscore the challenges in defining functional targets of RBPs since mere binding does not imply a discernible functional interaction., (© The Author(s) 2022. Published by Oxford University Press on behalf of NAR Cancer.)

Mutational landscape of CLL is now known to include recurrent non-synonymous mutations in SF3B1, a core splicing factor. About 5-10% of newly diagnosed CLL harbor these mutations which are typically limited to HEAT domains in the carboxyl-terminus of the protein. Importantly, the mutations are not specific to CLL but also present in several unrelated clonal disorders. Analysis of patient samples and cell lines has shown the primary splicing aberration in SF3B1-mutant cells to the use of novel or "cryptic" 3' splice sites (3SS). Advances in genome-editing and next-generation sequencing (NGS) have allowed development of isogenic models and detailed analysis of changes to the transcriptome with relative ease. In this manuscript, we focus on two relevant methods to study splicing factor mutations in CLL: development of isogenic scalable cell lines and informatics analysis of RNA-Seq datasets.

E2F-2 is a retinoblastoma (Rb)-regulated transcription factor induced during terminal erythroid maturation. Cyclin E-mediated Rb hyperphosphorylation induces E2F transcriptional activator functions. We previously reported that deregulated cyclin E activity causes defective terminal maturation of nucleated erythroblasts in vivo Here, we found that these defects are normalized by E2F-2 deletion; however, anemia in mice with deregulated cyclin E is not improved by E2F-2-loss, which itself causes reduced peripheral red blood cell (RBC) counts without altering relative abundances of erythroblast subpopulations. To determine how E2F-2 regulates RBC production, we comprehensively studied erythropoiesis using knockout mice and hematopoietic progenitors. We found that efficient stress erythropoiesis in vivo requires E2F-2, and we also identified an unappreciated role for E2F-2 in erythroblast enucleation. In particular, E2F-2 deletion impairs nuclear condensation, a morphological feature of maturing erythroblasts. Transcriptome profiling of E2F-2-null, mature erythroblasts demonstrated widespread changes in gene expression. Notably, we identified citron Rho-interacting kinase (CRIK), which has known functions in mitosis and cytokinesis, as induced in erythroblasts in an E2F-2-dependent manner, and we found that CRIK activity promotes efficient erythroblast enucleation and nuclear condensation. Together, our data reveal novel, lineage-specific functions for E2F-2 and suggest that some mitotic kinases have specialized roles supporting enucleation of maturing erythroblasts., (Copyright © 2016 American Society for Microbiology.)