Mangrove management in Sri Lanka and stakeholder collaboration: A social network perspective.

Understanding the extent of collaboration among stakeholders is key to supporting mangrove management. Despite the existence of robust policies, collaboration among stakeholders of mangrove co-management remains largely unexplored in Sri Lanka. This was partly due to the civil war, natural disasters, and other socio-economic changes over the past 30 years. Our study aimed to identify the collaboration between stakeholders of mangrove management and their perceptions regarding mangrove co-management in Sri Lanka using social network analysis and content analysis. Surveys were conducted in all five coastal provinces of Sri Lanka. Stakeholders included in the study were from government departments, non-governmental organizations, and private institutes. Our results showed that there were differences between coastal provinces in the mangrove management networks, specifically in the number of stakeholders involved and their degree of collaboration. Some important stakeholders (for example the Land Use and Policy Planning Department) were excluded from the social networks in certain provinces (Eastern and Western provinces). There were various issues hampering effective mangrove management such as inefficient communication, inconsistencies between policies, and insufficient financial capacity of government stakeholders responsible for policy implementation. According to the stakeholders in our study, providing mangrove management initiatives with long-term collaboration, post-care, continuous monitoring, and funding may help to overcome these challenges. Additionally, we suggest the establishment of a common platform to coordinate stakeholders. We further encourage increasing the participation of academics, researchers, and students from national universities in the mangrove co-management of Sri Lanka. Insights from this island-wide survey can be adapted to mangrove and other natural resource management trajectories in other countries as well.

DOT1L regulates chamber-specific transcriptional networks during cardiogenesis and mediates postnatal cell cycle withdrawal.

Mechanisms by which specific histone modifications regulate distinct gene networks remain little understood. We investigated how H3K79me2, a modification catalyzed by DOT1L and previously considered a general transcriptional activation mark, regulates gene expression during cardiogenesis. Embryonic cardiomyocyte ablation of Dot1l revealed that H3K79me2 does not act as a general transcriptional activator, but rather regulates highly specific transcriptional networks at two critical cardiogenic junctures: embryonic cardiogenesis, where it was particularly important for left ventricle-specific genes, and postnatal cardiomyocyte cell cycle withdrawal, with Dot1L mutants having more mononuclear cardiomyocytes and prolonged cardiomyocyte cell cycle activity. Mechanistic analyses revealed that H3K79me2 in two distinct domains, gene bodies and regulatory elements, synergized to promote expression of genes activated by DOT1L. Surprisingly, H3K79me2 in specific regulatory elements also contributed to silencing genes usually not expressed in cardiomyocytes. These results reveal mechanisms by which DOT1L successively regulates left ventricle specification and cardiomyocyte cell cycle withdrawal.

Differentiation of mouse fetal lung alveolar progenitors in serum-free organotypic cultures.

Lung epithelial progenitors differentiate into alveolar type 1 (AT1) and type 2 (AT2) cells. These cells form the air-blood interface and secrete surfactant, respectively, and are essential for lung maturation and function. Current protocols to derive and culture alveolar cells do not faithfully recapitulate the architecture of the distal lung, which influences cell fate patterns in vivo. Here, we report serum-free conditions that allow for growth and differentiation of mouse distal lung epithelial progenitors. We find that Collagen I promotes the differentiation of flattened, polarized AT1 cells. Using these organoids, we performed a chemical screen to investigate WNT signaling in epithelial differentiation. We identify an association between Casein Kinase activity and maintenance of an AT2 expression signature; Casein Kinase inhibition leads to an increase in AT1/progenitor cell ratio. These organoids provide a simplified model of alveolar differentiation and constitute a scalable screening platform to identify and analyze cell differentiation mechanisms.