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Migratory cells - either individually or in cohesive groups - are critical for spatiotemporally regulated processes such as embryonic development and wound healing. Their dysregulation is the underlying cause of formidable health problems such as congenital abnormalities and metastatic cancers. Border cell behavior during Drosophila oogenesis provides an effective model to study temporally regulated, collective cell migration in vivo. Developmental timing in flies is primarily controlled by the steroid hormone ecdysone, which acts through a well-conserved, nuclear hormone receptor complex. Ecdysone signaling determines the timing of border cell migration, but the molecular mechanisms governing this remain obscure. We found that border cell clusters expressing a dominantnegative form of ecdysone receptor extended ineffective protrusions. Additionally, these clusters had aberrant spatial distributions of E-cadherin (E-cad), apical domain markers and activated myosin that did not overlap. Remediating their expression or activity individually in clusters mutant for ecdysone signaling did not restore proper migration. We propose that ecdysone signaling synchronizes the functional distribution of E-cadherin, atypical protein kinase C (aPKC), Discs large (Dlg1) and activated myosin posttranscriptionally to coordinate adhesion, polarity and contractility and temporally control collective cell migration. [ABSTRACT FROM AUTHOR]

Cell migration is essential in animal development and co-opted during metastasis and inflammatory diseases. Some cells migrate collectively, which requires them to balance epithelial characteristics such as stable cell-cell adhesions with features of motility like rapid turnover of adhesions and dynamic cytoskeletal structures. How this is regulated is not entirely clear but important to understand. While investigating Drosophila oogenesis, we found that the putative E3 ubiquitin ligase, Mind bomb 2 (Mib2), is required to promote epithelial stability and the collective cell migration of border cells. Through biochemical analysis, we identified components of Mib2 complexes, which include E-cadherin and α- and β-catenins, as well as actin regulators. We also found that three Mib2 interacting proteins, RhoGAP19D, Supervillin, and Myosin heavy chain-like, affect border cell migration. mib2 mutant main body follicle cells have drastically reduced E-cadherin-based adhesion complexes and diminished actin filaments. We conclude that Mib2 acts to stabilize E-cadherin-based adhesion complexes and promote a robust actin cytoskeletal network, which is important for maintenance of epithelial integrity. The interaction with cadherin adhesion complexes and other cytoskeletal regulators contribute to its role in collective cell migration. Since Mib2 is well conserved, it may have similar functional significance in other organisms. [Display omitted] • Drosophila Mind bomb 2, an E3 ligase, is highly expressed in ovarian follicle cells. • mind bomb 2 is required for border cell migration and epithelial character. • Mind bomb 2 interactors, RhoGAP19D, Myosin heavy chain-like , and Supervillin , act in migration. • Loss of mind bomb 2 results in reduced adhesion complexes and F-actin. Summary statement: Mind bomb 2, an E3 ubiquitin ligase, enables collective cell migration in Drosophila and promotes epithelial character by stabilizing adhesion complexes and cytoskeletal proteins. [ABSTRACT FROM AUTHOR]

Chromatin insulators are DNA–protein complexes that promote specificity of enhancer–promoter interactions and maintain distinct transcriptional states through control of 3D genome organization. In this review, we highlight recent work visualizing how mammalian CCCTC-binding factor acts as a boundary to dynamic DNA loop extrusion mediated by cohesin. We also discuss new studies in both mammals and Drosophila that elucidate biological redundancy of chromatin insulator function and interplay with transcription with respect to topologically associating domain formation. Finally, we present novel concepts in spatiotemporal regulation of chromatin insulator function during differentiation and development and possible consequences of disrupted insulator activity on cellular proliferation. • Collision of cohesin with CTCF during loop extrusion can result in backtracking. • Drosophila chromatin insulator proteins act redundantly to form TAD borders. • Chromatin insulators and transcription together contribute to Drosophila TADs. • Delayed loop extrusion due to CTCF collision may serve as a developmental timer. [ABSTRACT FROM AUTHOR]

In this study, Leucaena leucocephala wood was pretreated with aqueous glycerol having H 2 SO 4 as the catalyst. Response surface methodology (RSM) and artificial neural network (ANN) were used to optimize the process parameters, catalyst concentration (1–3%), duration (120–300 min) and temperature (100–150 °C). ANN gave more accurate predictions for total reducing sugar yield than RSM. ANN also had lower values for error functions. Severity index (SI) was calculated based on the temperature, duration and catalyst concentration. Increase in SI from 0.21 * 10 3 to 2.06 * 10 3 increased total reducing sugar (TRS) production from 39.97 g/kg to 321.8 g/kg. Further increase in SI reduced the TRS and this change positively correlates with the loss of cellulose content. Correlation analysis showed that severity index can also be used to describe pretreatment process. [ABSTRACT FROM AUTHOR]

OBJECTIVES. The purpose of this work was to determine neurodevelopmental outcomes of preterm infants followed by a multidisciplinary team in a tertiary hospital in Bangladesh. METHODS. Infants <33 weeks' gestational age were serially assessed for neurodevelopment by physicians and developmental psychologists. An estimate of "low," "moderate," or "high" risk for neurodevelopmental impairments was made at the first visit. At later assessments, neurodevelopmental impairments were graded by severity as "none," "mild," or "serious." RESULTS. Of the 159 enrolled children, 65% survived, 16% died, and 19% were lost to follow-up. Family income was lowest among those who died, and maternal and paternal literacy was highest among the survivors. At a mean age of 31 months, developmental status of the 85 children followed-up for ≥ 12 months was normal in 32%; 45% had mild and 23% had serious neurodevelopmental impairments. Cognitive impairment was the most common deficit (60%). Final outcome was significantly better than estimated initially. Most serious (85%) but fewer mild (37%) problems were identified independently by both child health physicians and psychologists. CONCLUSIONS. Parental education and family income had significant influence on postdischarge mortality. Two thirds of infants demonstrated neurodevelopmental impairments. Most mild cognitive impairments would have been missed had either physicians or psychologists alone done the assessments. Preterm infants in this low-resource setting are at high risk for neurodevelopmental impairments, which need to be identified early, preferably by a multidisciplinary team of professionals. [ABSTRACT FROM AUTHOR]