Optimal taxonomic groups for biodiversity assessment: a meta‐analytic approach

A fundamental decision in biodiversity assessment is the selection of one or more study taxa, a choice that is often made using qualitative criteria such as historical precedent, ease of detection, or available technical or taxonomic expertise. A more robust approach would involve selecting taxa based on the a priori expectation that they will provide the best possible information on unmeasured groups, but data to inform such hypotheses are often lacking. Using a global meta‐analysis, we quantified the proportion of variability that each of 12 taxonomic groups (at the Order level or above) explained in the richness or composition of other taxa. We then applied optimization to matrices of pairwise congruency to identify the best set of complementary surrogate groups. We found that no single taxon was an optimal surrogate for both the richness and composition of unmeasured taxa if we used simple methods to aggregate congruence data between studies. In contrast, statistical methods that accounted for well‐known drivers of cross‐taxon congruence (spatial extent, grain size, and latitude) lead to the prioritization of similar surrogates for both species richness and composition. Advanced statistical methods were also more effective at describing known ecological relationships between taxa than simple methods, and show that congruence is typically highest between taxonomically and functionally dissimilar taxa. Birds and vascular plants were most frequently selected by our algorithm as surrogates for other taxonomic groups, but the extent to which any one taxon was the ‘optimal’ choice of surrogate for other biodiversity was highly context‐dependent. In the absence of other information – such as in data‐poor areas of the globe, and under limited budgets for monitoring or assessment – ecologists can use our results to assess which taxa are most likely to reflect the distribution of the richness or composition of ‘total’ biodiversity.     

Exploiting cell cycle inhibitor genes of the KRP family to control root‐knot nematode induced feeding sites in plants

Cell cycle control in galls provoked by root‐knot nematodes involves the activity of inhibitor genes like the Arabidopsis ICK/KRP members. Ectopic KRP1, KRP2 and KRP4 expression resulted in decreased gall size by inhibiting mitotic activity, whereas KRP6 induces mitosis in galls. Herein, we investigate the role of KRP3, KRP5 and KRP7 during gall development and compared their role with previously studied members of this class of cell cycle inhibitors. Overexpression of KRP3 and KRP7 culminated in undersized giant cells, with KRP3^OE galls presenting peculiar elongated giant cells. Nuclei in KRP3^OE and KRP5^OE lines presented a convoluted and apparently connected phenotype. This appearance may be associated with the punctuated protein nuclear localization driven by specific common motifs. As well, ectopic expression of KRP3^OE and KRP5^OE affected nematode development and offspring. Decreased mitotic activity in galls of KRP3^OE and KRP7^OE lines led to a reduced gall size which presented distinct shapes – from more elongated like in the KRP3^OE line to small rounded like in the KRP7^OE line. Results presented strongly support the idea that induced expression of cell cycle inhibitors such as KRP3 and KRP7 in galls can be envisaged as a conceivable strategy for nematode feeding site control in crop species attacked by phytopathogenic nematodes.     

Increased oxidative stress alters nucleosides metabolite levels in sickle cell anemia

Objectives: This study was conducted to assess the markers of oxidative stress, myeloperoxidase (MPO), acetylcholinesterase (AChE) and xanthine oxidase (XO) activities as well as the levels of nucleotide metabolites in sickle cell anemia (SCA) patients.

Methods: Fifteen SCA treated patients and 30 health subjects (control group) were selected. The markers of oxidative stress (levels of reactive oxygen species (ROS), plasma proteins, carbonyl content, lipid peroxidation (TBARS), total thiols (T-SH), glutathione and catalase activity), MPO, AChE and XO activities as well as the levels of nucleotide metabolites were measured in SCA patients.

Results: ROS, thiobarbituric acid-reactive substances (TBARS) and T-SH levels as well as the activities of catalase and MPO were significantly increased while glutathione level was reduced in SCA patients. Furthermore, a significant (P?P?P?P?Discussion: The altered parameters in SCA patients suggest that the generation and impairment of oxidative stress in this disease as well as antioxidant markers are contributory factors towards cellular redox homeostasis and alteration of purine metabolites.     

Misoprostol treatment prevents hypoxia-induced cardiac dysfunction through a 14-3-3 and PKA regulatory motif on Bnip3

Systemic hypoxia is a common element in most perinatal emergencies and is a known driver of Bnip3 expression in the neonatal heart. Bnip3 plays a prominent role in the evolution of necrotic cell death, disrupting ER calcium homeostasis and initiating mitochondrial permeability transition (MPT). Emerging evidence suggests a cardioprotective role for the prostaglandin E1 analog misoprostol during periods of hypoxia, but the mechanisms for this protection are not completely understood. Using a combination of mouse and cell models, we tested if misoprostol is cardioprotective during neonatal hypoxic injury by altering Bnip3 function. Here we report that hypoxia elicits mitochondrial-fragmentation, MPT, reduced ejection fraction, and evidence of necroinflammation, which were abrogated with misoprostol treatment or Bnip3 knockout. Through molecular studies we show that misoprostol leads to PKA-dependent Bnip3 phosphorylation at threonine-181, and subsequent redistribution of Bnip3 from mitochondrial Opa1 and the ER through an interaction with 14-3-3 proteins. Taken together, our results demonstrate a role for Bnip3 phosphorylation in the regulation of cardiomyocyte contractile/metabolic dysfunction, and necroinflammation. Furthermore, we identify a potential pharmacological mechanism to prevent neonatal hypoxic injury.Subject terms: Cell death, Cardiovascular biology     

Genomic Epidemiology of SARS-CoV-2 in Pakistan

COVID-19 has swept globally and Pakistan is no exception. To investigate the initial introductions and transmissions of the SARS-CoV-2 in Pakistan, we performed the largest genomic epidemiology study of COVID-19 in Pakistan and generated 150 complete SARS-CoV-2 genome sequences from samples collected from March 16 to June 1, 2020. We identified a total of 347 mutated positions, 31 of which were over-represented in Pakistan. Meanwhile, we found over 1000 intra-host single-nucleotide variants (iSNVs). Several of them occurred concurrently, indicating possible interactions among them or coevolution. Some of the high-frequency iSNVs in Pakistan were not observed in the global population, suggesting strong purifying selections. The genomic epidemiology revealed five distinctive spreading clusters. The largest cluster consisted of 74 viruses which were derived from different geographic locations of Pakistan and formed a deep hierarchical structure, indicating an extensive and persistent nation-wide transmission of the virus that was probably attributed to a signature mutation (G8371T in ORF1ab) of this cluster. Furthermore, 28 putative international introductions were identified, several of which are consistent with the epidemiological investigations. In all, this study has inferred the possible pathways of introductions and transmissions of SARS-CoV-2 in Pakistan, which could aid ongoing and future viral surveillance and COVID-19 control.