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Drought tolerant maize (Zea mays L.) hybrids are crucial for the sustainability of maize production in the drought-prone areas of Sub-saharan Africa. Understanding the genetics of inheritance under drought is important in designing breeding strategies for improving grain yield and other agronomic traits under drought. Two studies were conducted to determine the the genetic variability and mode of gene action for grain yield and other traits of different maturity groups of maize inbreds for tolerance to drought and identify the promising drought-tolerant maize hybrid(s) for drought-prone regions. Eleven inbred lines of different maturity groups and endosperm-modification were crossed using diallel mating scheme to generate 55 F1 hybrids. The 55 hybrids along with one check and 11 inbreds were separately evaluated under induced drought and optimum growing conditions at Samaru and Kadawa. The experiments were laid in a 7 x 8 alpha lattice design and replicated two times using single-row plot of 4-m long. Row and hill spacing were 0.75 m and 0.4 m respectively. General combining ability (GCA) and Specific combining ability (SCA) mean squares were significant (p < 0.01) for grain yield and most other traits under drought and optimum growing conditions. SCA accounted for 79.3% and 64.2% of the total genetic variation for grain yield under drought and optimum growing conditions, indicating that non-additive gene action largely controlled the inheritance of grain yield of the hybrids. Hybrid TZEE-W-Pop STR C5 x TZEI 87 should be further tested in multiple environments for adoption by farmers in drought prone areas of Sub-saharan Africa. [ABSTRACT FROM AUTHOR]

Advances in genome sequencing have improved our understanding of the genetic basis of human diseases, and thousands of human genes have been associated with different diseases. Recent genomic adaptation at disease genes has not been well characterized. Here, we compare the rate of strong recent adaptation in the form of selective sweeps between mendelian, non-infectious disease genes and non-disease genes across distinct human populations from the 1000 Genomes Project. We find that mendelian disease genes have experienced far less selective sweeps compared to non-disease genes especially in Africa. Investigating further the possible causes of the sweep deficit at disease genes, we find that this deficit is very strong at disease genes with both low recombination rates and with high numbers of associated disease variants, but is almost non-existent at disease genes with higher recombination rates or lower numbers of associated disease variants. Because segregating recessive deleterious variants have the ability to interfere with adaptive ones, these observations strongly suggest that adaptation has been slowed down by the presence of interfering recessive deleterious variants at disease genes. These results suggest that disease genes suffer from a transient inability to adapt as fast as the rest of the genome. [ABSTRACT FROM AUTHOR]

While it is generally accepted that language and speech have genetic foundations, and that the widespread inter-individual variation observed in many of their aspects is partly driven by variation in genes, it is much less clear if differences between languages may also be partly rooted in our genes. One such proposal is that the population frequencies of the so-called "derived" alleles of two genes involved in brain growth and development, ASPM and Microcephalin, are related to the probability of speaking a tone language or not. The original study introducing this proposal used a cross-linguistic statistical approach, showing that these associations are "special" when compared with many other possible relationships between genetic variants and linguistic features. Recent experimental evidence supports strongly a negative effect of the "derived" allele of ASPM on tone perception and/or processing within individuals, but failed to find any effect for Microcephalin. Motivated by these experimental findings, I conduct here a cross-linguistic statistical test, using a larger and updated dataset of 175 samples from 129 unique (meta)populations, and a battery of methods including mixed-effects regression (Bayesian and maximum-likelihood), mediation and path analysis, decision trees and random forests, using permutations and restricted sampling to control for the confounding effects of genealogy (language families) and contact (macroareas). Overall, the results support a negative weak effect of ASPM-D against the presence of tone above and beyond the strong confounding influences of genealogy and contact, but they suggest that the original association between tone and MCPH1 might have been a false positive, explained by differences between populations and languages within and outside Africa. Thus, these cross-linguistic population-scale statistical results are fully consonant with the inter-individual-level experimental results, and suggest that the observed linguistic diversity may be, at least in some cases, partly driven by genetic diversity. [ABSTRACT FROM AUTHOR]

Early-onset diabetes is poorly diagnosed partly due to its heterogeneity and variable presentations. Although several genes have been associated with the disease, these genes are not well studied in Africa. We sought to identify the major neonatal, early childhood, juvenile, or early-onset diabetes genes in Africa; and evaluate the available molecular methods used for investigating these gene variants. A literature search was conducted on PubMed, Scopus, Africa-Wide Information, and Web of Science databases. The retrieved records were screened and analyzed to identify genetic variants associated with early-onset diabetes. Although 319 records were retrieved, 32 were considered for the current review. Most of these records (22/32) were from North Africa. The disease condition was genetically heterogenous with most cases possessing unique gene variants. We identified 22 genes associated with early-onset diabetes, 9 of which had variants (n = 19) classified as pathogenic or likely pathogenic (PLP). Among the PLP variants, IER3IP1 : p.(Leu78Pro) was the variant with the highest number of cases. There was limited data from West Africa, hence the contribution of genetic variability to early-onset diabetes in Africa could not be comprehensively evaluated. It is worth mentioning that most studies were focused on natural products as antidiabetics and only a few studies reported on the genetics of the disease. ABCC8 and KCNJ11 were implicated as major contributors to early-onset diabetes gene networks. Gene ontology analysis of the network associated ion channels, impaired glucose tolerance, and decreased insulin secretions to the disease. Our review highlights 9 genes from which PLP variants have been identified and can be considered for the development of an African diagnostic panel. There is a gap in early-onset diabetes genetic research from sub-Saharan Africa which is much needed to develop a comprehensive, efficient, and cost-effective genetic panel that will be useful in clinical practice on the continent and among the African diasporas. [ABSTRACT FROM AUTHOR]

Recent sequencing of Plasmodium vivax field isolates and monkey-adapted strains enabled characterization of SNPs throughout the genome. These analyses relied on mapping short reads onto the P. vivax reference genome that was generated using DNA from the monkey-adapted strain Salvador I. Any genomic locus deleted in this strain would be lacking in the reference genome sequence and missed in previous analyses. Here, we report de novo assembly of a P. vivax field isolate genome. Out of 2,857 assembled contigs, we identify 362 contigs, each containing more than 5 kb of contiguous DNA sequences absent from the reference genome sequence. These novel P. vivax DNA sequences account for 3.8 million nucleotides and contain 792 predicted genes. Most of these contigs contain members of multigene families and likely originate from telomeric regions. Interestingly, we identify two contigs containing predicted protein coding genes similar to known Plasmodium red blood cell invasion proteins. One gene encodes the reticulocyte-binding protein gene orthologous to P. cynomolgi RBP2e and P. knowlesi NBPXb. The second gene harbors all the hallmarks of a Plasmodium erythrocyte-binding protein, including conserved Duffy-binding like and C-terminus cysteine-rich domains. Phylogenetic analysis shows that this novel gene clusters separately from all known Plasmodium Duffy-binding protein genes. Additional analyses showing that this gene is present in most P. vivax genomes and transcribed in blood-stage parasites suggest that P. vivax red blood cell invasion mechanisms may be more complex than currently understood. The strategy employed here complements previous genomic analyses and takes full advantage of next-generation sequencing data to provide a comprehensive characterization of genetic variations in this important malaria parasite. Further analyses of the novel protein coding genes discovered through de novo assembly have the potential to identify genes that influence key aspects of P. vivax biology, including alternative mechanisms of human erythrocyte invasion. Author Summary: Plasmodium vivax is responsible for most malaria cases outside Africa, but is poorly understood, as the parasite is difficult to study in vitro. Genome sequencing studies offer a novel and exciting opportunity to better understand this parasite but, so far, have directly mapped reads onto the reference genome sequence generated from a single P. vivax strain. Here, we use sequence data generated from a field isolate to reconstruct long DNA sequences without relying on the reference genome. Our analyses reveal many P. vivax DNA sequences that are absent from the reference genome and contain 792 predicted genes. One of these novel genes encodes a predicted protein similar to known Plasmodium proteins involved in red blood cell invasion. This new gene is present in all P. vivax strains sequenced so far, except for the strain used to generate the reference genome, and is transcribed in blood-stage parasites. Overall, our analyses show that the catalogue of P. vivax genes was incomplete and that potentially important genes have been missed. We notably identified one putative invasion gene that seems functional and could dramatically change our understanding of the mechanisms determining red blood cell invasion by this important malaria parasite. [ABSTRACT FROM AUTHOR]

Identifying regions of the human genome that have been targets of natural selection will provide important insights into human evolutionary history and may facilitate the identification of complex disease genes. Although the signature that natural selection imparts on DNA sequence variation is difficult to disentangle from the effects of neutral processes such as population demographic history, selective and demographic forces can be distinguished by analyzing multiple loci dispersed throughout the genome. We studied the molecular evolution of 132 genes by comprehensively resequencing them in 24 African-Americans and 23 European-Americans. We developed a rigorous computational approach for taking into account multiple hypothesis tests and demographic history and found that while many apparent selective events can instead be explained by demography, there is also strong evidence for positive or balancing selection at eight genes in the European-American population, but none in the African-American population. Our results suggest that the migration of modern humans out of Africa into new environments was accompanied by genetic adaptations to emergent selective forces. In addition, a region containing four contiguous genes on Chromosome 7 showed striking evidence of a recent selective sweep in European-Americans. More generally, our results have important implications for mapping genes underlying complex human diseases. An analysis of 132 human genes suggests that the migration of modern humans out of Africa into new environments was accompanied by genetic adaptations to emergent selective forces. [ABSTRACT FROM AUTHOR]