Zhaohui Fu, Tao Tang and Jiang Yang
Math. Comp. 93 (), 2745-2767.
Abstract, references and article information

Tim Chumley explains the connections between random billiards and the science of heat and energy transfer. If you've ever played billiards or pool, you've used your intuition and some mental geometry to plan your shots. Mathematicians have gone a step further, using these games as inspiration for new mathematical problems. Starting from the simple theoretical setup of a single ball bouncing around in an enclosed region, the possibilities are endless. For instance, if the region is shaped like a stadium (a rectangle with semicircles on opposite sides), and several balls start moving with nearly the same velocity and position, their paths in the region soon differ wildly: chaos. Mathematical billiards even have connections to thermodynamics, the branch of physics dealing with heat, temperature, and energy transfer.

Dr. Valentina Wheeler of University of Wollongong, Australia, shares how her work influences efforts to understand wildfires and red blood cells. In Australia, where bushfires are a concern year-round, researchers have long tried to model these wildfires, hoping to learn information that can help with firefighting policy. Mathematician Valentina Wheeler and colleagues began studying a particularly dangerous phenomenon: When two wildfires meet, they create a new, V-shaped fire whose pointed tip races along to catch up with the two branches of the V, moving faster than either of the fires alone. This is exactly what happens in a mathematical process known as mean curvature flow. Mean curvature flow is a process in which a shape smooths out its boundaries over time. Just as with wildfires, pointed corners and sharp bumps will change the fastest.

Yinji Li, Zhiwei Wang and Xiangyu Zhou
Trans. Amer. Math. Soc. 377 (), 5947-5992.
Abstract, references and article information

Jong In Han and Sijong Kwak
Trans. Amer. Math. Soc. 377 (), 5561-5581.
Abstract, references and article information

Noga Alon, Anurag Bishnoi, Shagnik Das and Alessandro Neri
Trans. Amer. Math. Soc. 377 (), 5389-5410.
Abstract, references and article information

Denise Uwamariya and Xiangfeng Yang
Theor. Probability and Math. Statist. 111 (), 167-179.
Abstract, references and article information

Claudio Macci and Barbara Pacchiarotti
Theor. Probability and Math. Statist. 111 (), 21-43.
Abstract, references and article information

Abdessamad Dehaj and Mohamed Guessous
Theor. Probability and Math. Statist. 111 (), 1-8.
Abstract, references and article information

Lasse L. Wolf and Hong-Wei Zhang
Proc. Amer. Math. Soc. 152 (), 5445-5453.
Abstract, references and article information

Shengyu Tang
Proc. Amer. Math. Soc. 152 (), 5381-5394.
Abstract, references and article information

Anh Tuan Nguyen, Tómas Caraballo and Nguyen Huy Tuan
Proc. Amer. Math. Soc. 152 (), 5175-5189.
Abstract, references and article information

Donghyeok Lim and Christian Maire
Proc. Amer. Math. Soc. 152 (), 5013-5024.
Abstract, references and article information

Naoki Endo and Shiro Goto
Proc. Amer. Math. Soc. 152 (), 5007-5011.
Abstract, references and article information

T. A. Suslina
St. Petersburg Math. J. 35 (), 537-570.
Abstract, references and article information

P. Lochak
St. Petersburg Math. J. 35 (), 477-535.
Abstract, references and article information

The Math Community Educational Outreach (Math CEO) program at the University of California, Irvine (UCI) will receive the 2025 AMS Award for an Exemplary Program or Achievement in a Mathematics Department.

Founded in 2014, UCI’s Math CEO is an after-school math enrichment program aimed at increasing the number of talented students in STEM from diverse backgrounds by fostering mathematical exploration, mentor development, and community engagement.

From the citation

The University of California, Irvine (UCI) Math CEO program is recognized for its exceptional contributions to the mathematics community and society at large. Established in 2014 by professors Alessandra Pantano and Li-Sheng Tseng, Math CEO targets students from Title I middle schools, providing them with a high-quality after-school math enrichment program. This program brings middle-school students to the UCI campus to work in small groups with undergraduate mentors, many of whom are also from historically marginalized groups, to engage in challenging mathematical tasks and encourage exploration. 

From September 2019 to June 2024, Math CEO engaged a total of 1,221 youth, with 48.6% identifying as female. The ethnic background of the participants was predominantly Latinx (93.5%), with smaller representations of Asian, white, and multiethnic students. In the same five-year period, Math CEO engaged 553 undergraduate mentors, 62.2% of whom were female. The mentors’ ethnic backgrounds were diverse, with significant representation of Asian (52%) and Latinx (30%) students. The undergraduate mentors, many of whom pursue careers in education, receive training in culturally responsive teaching practices and equity in education, significantly impacting their professional development. In a post-survey, 52.3% of the undergraduate mentors expressed interest in teaching or working in education and 45.9% were likely to pursue professions working with children or families.

Recognizing the central role of families in supporting Latinx youth, Math CEO involves parents through bilingual workshops that enhance community awareness of college pathways and financial opportunities. 

Math CEO has been the foundation for numerous research projects in mathematics education, supported by NSF grants, leading to publications and program growth. The program’s success is evident in its expansion to high schools and other regions in Southern California, including a new branch at California State University, Dominguez Hills. Math CEO continues to make a substantial impact on underserved youth, demonstrating a model of systemic, reproducible change that can be implemented by others.

Response of Alessandra Pantano, UCI Math CEO

I am deeply honored to receive the AMS Award for an Exemplary Program in a Mathematics Department on behalf of the UCI Math CEO team. This wonderful award recognizes the work of many colleagues, graduate students, and undergraduate students in developing and delivering the UCI Math Community Educational Outreach (Math CEO) program. For over a decade, Math CEO has provided creative and culturally responsive math enrichment opportunities for hundreds of underprivileged middle-school students, many of which have since “graduated” to high school or even college. Leading this exceptional and dedicated team of volunteers has been the highest pride of my professional life. A special thanks to my partners-in-crime, Prof. Li-Sheng Tseng, codirector of Math CEO, and former graduate student Andres Forero Cuervo, academic coordinator for Math CEO: We could have never done this without you. I look forward to pushing this activity forward and continuing to dedicate my energy to help kids in our county find the way to express their potential – in math and in life! A big thanks to the colleagues who nominated us and to the AMS for recognizing our efforts.  

History of the program

The UC Irvine Math Community Educational Outreach (Math CEO) program was founded in 2014 by math faculty Alessandra Pantano and Li-Sheng Tseng in collaboration with Santa Ana Unified math teacher Jasmina Matasovic. The founders shared a belief that low standardized test scores in underserved communities do not reflect students’ interest and potential to succeed in STEM. Math CEO runs free, weekly, after-school math enrichment sessions, welcoming all youth regardless of math achievement. Starting with only 25 students from one middle school, the program has grown and engaged nearly two thousand students in all, from multiple school districts in Southern California.

About the award

The annual AMS Award for an Exemplary Program or Achievement in a Mathematics Department was established in 2004 and first given in 2006. This award recognizes a department which has distinguished itself by undertaking an unusual or particularly effective program of value to the mathematics community, internally or in relation to the rest of society. Departments of mathematical sciences in North America that offer at least a bachelor’s degree in mathematical sciences are eligible. The award amount is currently $5,000. The award will be presented at the 2025 Joint Mathematics Meetings in Seattle.

Learn more about the award and previous recipients.

Contact: AMS Communications.

*****

The American Mathematical Society is dedicated to advancing research and connecting the diverse global mathematical community through our publications, meetings and conferences, MathSciNet, professional services, advocacy, and awareness programs.
 

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Knockout mouse models have been extensively used to study the antiviral activity of IFIT (interferon-induced protein with tetratricopeptide repeats). Human IFIT1 binds to cap0 (m7GpppN) RNA, which lacks methylation on the first and second cap-proximal nucleotides (cap1, m7GpppNm, and cap2, m7GpppNmNm, respectively). These modifications are signatures of “self” in higher eukaryotes, whereas unmodified cap0-RNA is recognized as foreign and, therefore, potentially harmful to the host cell. IFIT1 inhibits translation at the initiation stage by competing with the cap-binding initiation factor complex, eIF4F, restricting infection by certain viruses that possess “nonself” cap0-mRNAs. However, in mice and other rodents, the IFIT1 orthologue has been lost, and the closely related Ifit1b has been duplicated twice, yielding three paralogues: Ifit1, Ifit1b, and Ifit1c. Although murine Ifit1 is similar to human IFIT1 in its cap0-RNA–binding selectivity, the roles of Ifit1b and Ifit1c are unknown. Here, we found that Ifit1b preferentially binds to cap1-RNA, whereas binding is much weaker to cap0- and cap2-RNA. In murine cells, we show that Ifit1b can modulate host translation and restrict WT mouse coronavirus infection. We found that Ifit1c acts as a stimulatory cofactor for both Ifit1 and Ifit1b, promoting their translation inhibition. In this way, Ifit1c acts in an analogous fashion to human IFIT3, which is a cofactor to human IFIT1. This work clarifies similarities and differences between the human and murine IFIT families to facilitate better design and interpretation of mouse models of human infection and sheds light on the evolutionary plasticity of the IFIT family.

Distinct cell types emerge from embryonic stem cells through a precise and coordinated execution of gene expression programs during lineage commitment. This is established by the action of lineage specific transcription factors along with chromatin complexes. Numerous studies have focused on epigenetic factors that affect embryonic stem cells (ESC) self-renewal and pluripotency. However, the contribution of chromatin to lineage decisions at the exit from pluripotency has not been as extensively studied. Using a pooled epigenetic shRNA screen strategy, we identified chromatin-related factors critical for differentiation toward mesodermal and endodermal lineages. Here we reveal a critical role for the chromatin protein, ARID4B. Arid4b-deficient mESCs are similar to WT mESCs in the expression of pluripotency factors and their self-renewal. However, ARID4B loss results in defects in up-regulation of the meso/endodermal gene expression program. It was previously shown that Arid4b resides in a complex with SIN3A and HDACS 1 and 2. We identified a physical and functional interaction of ARID4B with HDAC1 rather than HDAC2, suggesting functionally distinct Sin3a subcomplexes might regulate cell fate decisions Finally, we observed that ARID4B deficiency leads to increased H3K27me3 and a reduced H3K27Ac level in key developmental gene loci, whereas a subset of genomic regions gain H3K27Ac marks. Our results demonstrate that epigenetic control through ARID4B plays a key role in the execution of lineage-specific gene expression programs at pluripotency exit.

Thoracic great vessels such as the aorta and subclavian arteries are formed through dynamic remodeling of embryonic pharyngeal arch arteries (PAAs). Previous work has shown that loss of a basic helix-loop-helix transcription factor Hey1 in mice causes abnormal fourth PAA development and lethal great vessel anomalies resembling congenital malformations in humans. However, how Hey1 mediates vascular formation remains unclear. In this study, we revealed that Hey1 in vascular endothelial cells, but not in smooth muscle cells, played essential roles for PAA development and great vessel morphogenesis in mouse embryos. Tek-Cre–mediated Hey1 deletion in endothelial cells affected endothelial tube formation and smooth muscle differentiation in embryonic fourth PAAs and resulted in interruption of the aortic arch and other great vessel malformations. Cell specificity and signal responsiveness of Hey1 expression were controlled through multiple cis-regulatory regions. We found two distal genomic regions that had enhancer activity in endothelial cells and in the pharyngeal epithelium and somites, respectively. The novel endothelial enhancer was conserved across species and was specific to large-caliber arteries. Its transcriptional activity was regulated by Notch signaling in vitro and in vivo, but not by ALK1 signaling and other transcription factors implicated in endothelial cell specificity. The distal endothelial enhancer was not essential for basal Hey1 expression in mouse embryos but may likely serve for Notch-dependent transcriptional control in endothelial cells together with the proximal regulatory region. These findings help in understanding the significance and regulation of endothelial Hey1 as a mediator of multiple signaling pathways in embryonic vascular formation.

Clostridium difficile is an anaerobic and spore-forming bacterium responsible for 15–25% of postantibiotic diarrhea and 95% of pseudomembranous colitis. Peptidoglycan is a crucial element of the bacterial cell wall that is exposed to the host, making it an important target for the innate immune system. The C. difficile peptidoglycan is largely N-deacetylated on its glucosamine (93% of muropeptides) through the activity of enzymes known as N-deacetylases, and this N-deacetylation modulates host–pathogen interactions, such as resistance to the bacteriolytic activity of lysozyme, virulence, and host innate immune responses. C. difficile genome analysis showed that 12 genes potentially encode N-deacetylases; however, which of these N-deacetylases are involved in peptidoglycan N-deacetylation remains unknown. Here, we report the enzymes responsible for peptidoglycan N-deacetylation and their respective regulation. Through peptidoglycan analysis of several mutants, we found that the N-deacetylases PdaV and PgdA act in synergy. Together they are responsible for the high level of peptidoglycan N-deacetylation in C. difficile and the consequent resistance to lysozyme. We also characterized a third enzyme, PgdB, as a glucosamine N-deacetylase. However, its impact on N-deacetylation and lysozyme resistance is limited, and its physiological role remains to be dissected. Finally, given the influence of peptidoglycan N-deacetylation on host defense against pathogens, we investigated the virulence and colonization ability of the mutants. Unlike what has been shown in other pathogenic bacteria, a lack of N-deacetylation in C. difficile is not linked to a decrease in virulence.

Infiltration of peripheral immune cells after blood-brain barrier dysfunction causes severe inflammation after a stroke. Although the endothelial glycocalyx, a network of membrane-bound glycoproteins and proteoglycans that covers the lumen of endothelial cells, functions as a barrier to circulating cells, the relationship between stroke severity and glycocalyx dysfunction remains unclear. In this study, glycosaminoglycans, a component of the endothelial glycocalyx, were studied in the context of ischemic stroke using a photochemically induced thrombosis mouse model. Decreased levels of heparan sulfate and chondroitin sulfate and increased activity of hyaluronidase 1 and heparanase (HPSE) were observed in ischemic brain tissues. HPSE expression in cerebral vessels increased after stroke onset and infarct volume greatly decreased after co-administration of N-acetylcysteine + glycosaminoglycan oligosaccharides as compared with N-acetylcysteine administration alone. These results suggest that the endothelial glycocalyx was injured after the onset of stroke. Interestingly, scission activity of proHPSE produced by immortalized endothelial cells and HEK293 cells transfected with hHPSE1 cDNA were activated by acrolein (ACR) exposure. We identified the ACR-modified amino acid residues of proHPSE using nano LC–MS/MS, suggesting that ACR modification of Lys139 (6-kDa linker), Lys107, and Lys161, located in the immediate vicinity of the 6-kDa linker, at least in part is attributed to the activation of proHPSE. Because proHPSE, but not HPSE, localizes outside cells by binding with heparan sulfate proteoglycans, ACR-modified proHPSE represents a promising target to protect the endothelial glycocalyx.

VAR2CSA is the placental-malaria–specific member of the antigenically variant Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1) family. It is expressed on the surface of Plasmodium falciparum-infected host red blood cells and binds to specific chondroitin-4-sulfate chains of the placental proteoglycan receptor. The functional ∼310 kDa ectodomain of VAR2CSA is a multidomain protein that requires a minimum 12-mer chondroitin-4-sulfate molecule for specific, high affinity receptor binding. However, it is not known how the individual domains are organized and interact to create the receptor-binding surface, limiting efforts to exploit its potential as an effective vaccine or drug target. Using small angle X-ray scattering and single particle reconstruction from negative-stained electron micrographs of the ectodomain and multidomain constructs, we have determined the structural architecture of VAR2CSA. The relative locations of the domains creates two distinct pores that can each accommodate the 12-mer of chondroitin-4-sulfate, suggesting a model for receptor binding. This model has important implications for understanding cytoadherence of infected red blood cells and potentially provides a starting point for developing novel strategies to prevent and/or treat placental malaria.

Cation diffusion facilitator (CDF) proteins are a conserved family of divalent transition metal cation transporters. CDF proteins are usually composed of two domains: the transmembrane domain, in which the metal cations are transported through, and a regulatory cytoplasmic C-terminal domain (CTD). Each CDF protein transports either one specific metal or multiple metals from the cytoplasm, and it is not known whether the CTD takes an active regulatory role in metal recognition and discrimination during cation transport. Here, the model CDF protein MamM, an iron transporter from magnetotactic bacteria, was used to probe the role of the CTD in metal recognition and selectivity. Using a combination of biophysical and structural approaches, the binding of different metals to MamM CTD was characterized. Results reveal that different metals bind distinctively to MamM CTD in terms of their binding sites, thermodynamics, and binding-dependent conformations, both in crystal form and in solution, which suggests a varying level of functional discrimination between CDF domains. Furthermore, these results provide the first direct evidence that CDF CTDs play a role in metal selectivity. We demonstrate that MamM's CTD can discriminate against Mn2+, supporting its postulated role in preventing magnetite formation poisoning in magnetotactic bacteria via Mn2+ incorporation.

Connexin (Cx) protein forms hemichannels and gap junctional channels, which play diverse and profound roles in human physiology and diseases. Gap junctions are arrays of intercellular channels formed by the docking of two hemichannels from adjacent cells. Each hexameric hemichannel contains the same or different Cx isoform. Although homomeric Cxs forms have been largely described functionally and structurally, the stoichiometry and arrangement of heteromeric Cx channels remain unknown. The latter, however, are widely expressed in human tissues and variation might have important implications on channel function. Investigating properties of heteromeric Cx channels is challenging considering the high number of potential subunit arrangements and stoichiometries, even when only combining two Cx isoforms. To tackle this problem, we engineered an HA tag onto Cx26 or Cx30 subunits and imaged hemichannels that were liganded by Fab-epitope antibody fragments via atomic force microscopy. For Cx26-HA/Cx30 or Cx30-HA/Cx26 heteromeric channels, the Fab-HA binding distribution was binomial with a maximum of three Fab-HA bound. Furthermore, imaged Cx26/Cx30-HA triple liganded by Fab-HA showed multiple arrangements that can be derived from the law of total probabilities. Atomic force microscopy imaging of ringlike structures of Cx26/Cx30-HA hemichannels confirmed these findings and also detected a polydisperse distribution of stoichiometries. Our results indicate a dominant subunit stoichiometry of 3Cx26:3Cx30 with the most abundant subunit arrangement of Cx26-Cx26-Cx30-Cx26-Cx30-Cx30. To our knowledge, this is the first time that the molecular architecture of heteromeric Cx channels has been revealed, thus providing the basis to explore the functional effect of these channels in biology.

Identification of antibody-binding epitopes is crucial to understand immunological mechanisms. It is of particular interest for allergenic proteins with high cross-reactivity as observed in the lipid transfer protein (LTP) syndrome, which is characterized by severe allergic reactions. Art v 3, a pollen LTP from mugwort, is frequently involved in this cross-reactivity, but no antibody-binding epitopes have been determined so far. To reveal human IgE-binding regions of Art v 3, we produced three murine high-affinity mAbs, which showed 70–90% coverage of the allergenic epitopes from mugwort pollen–allergic patients. As reliable methods to determine structural epitopes with tightly interacting intact antibodies under native conditions are lacking, we developed a straightforward NMR approach termed hydrogen/deuterium exchange memory (HDXMEM). It relies on the slow exchange between the invisible antigen-mAb complex and the free 15N-labeled antigen whose 1H-15N correlations are detected. Due to a memory effect, changes of NH protection during antibody binding are measured. Differences in H/D exchange rates and analyses of mAb reactivity to homologous LTPs revealed three structural epitopes: two partially cross-reactive regions around α-helices 2 and 4 as well as a novel Art v 3–specific epitope at the C terminus. Protein variants with exchanged epitope residues confirmed the antibody-binding sites and revealed strongly reduced IgE reactivity. Using the novel HDXMEM for NMR epitope mapping allowed identification of the first structural epitopes of an allergenic pollen LTP. This knowledge enables improved cross-reactivity prediction for patients suffering from LTP allergy and facilitates design of therapeutics.

Arabinogalactan proteins (AGPs) are plant proteoglycans with functions in growth and development. However, these functions are largely unexplored, mainly because of the complexity of the sugar moieties. These carbohydrate sequences are generally analyzed with the aid of glycoside hydrolases. The exo-β-1,3-galactanase is a glycoside hydrolase from the basidiomycete Phanerochaete chrysosporium (Pc1,3Gal43A), which specifically cleaves AGPs. However, its structure is not known in relation to its mechanism bypassing side chains. In this study, we solved the apo and liganded structures of Pc1,3Gal43A, which reveal a glycoside hydrolase family 43 subfamily 24 (GH43_sub24) catalytic domain together with a carbohydrate-binding module family 35 (CBM35) binding domain. GH43_sub24 is known to lack the catalytic base Asp conserved among other GH43 subfamilies. Our structure in combination with kinetic analyses reveals that the tautomerized imidic acid group of Gln263 serves as the catalytic base residue instead. Pc1,3Gal43A has three subsites that continue from the bottom of the catalytic pocket to the solvent. Subsite −1 contains a space that can accommodate the C-6 methylol of Gal, enabling the enzyme to bypass the β-1,6–linked galactan side chains of AGPs. Furthermore, the galactan-binding domain in CBM35 has a different ligand interaction mechanism from other sugar-binding CBM35s, including those that bind galactomannan. Specifically, we noted a Gly → Trp substitution, which affects pyranose stacking, and an Asp → Asn substitution in the binding pocket, which recognizes β-linked rather than α-linked Gal residues. These findings should facilitate further structural analysis of AGPs and may also be helpful in engineering designer enzymes for efficient biomass utilization.

Programmed ribosomal frameshifting (PRF) is a mechanism used by arteriviruses like porcine reproductive and respiratory syndrome virus (PRRSV) to generate multiple proteins from overlapping reading frames within its RNA genome. PRRSV employs −1 PRF directed by RNA secondary and tertiary structures within its viral genome (canonical PRF), as well as a noncanonical −1 and −2 PRF that are stimulated by the interactions of PRRSV nonstructural protein 1β (nsp1β) and host protein poly(C)-binding protein (PCBP) 1 or 2 with the viral genome. Together, nsp1β and one of the PCBPs act as transactivators that bind a C-rich motif near the shift site to stimulate −1 and −2 PRF, thereby enabling the ribosome to generate two frameshift products that are implicated in viral immune evasion. How nsp1β and PCBP associate with the viral RNA genome remains unclear. Here, we describe the purification of the nsp1β:PCBP2:viral RNA complex on a scale sufficient for structural analysis using small-angle X-ray scattering and stochiometric analysis by analytical ultracentrifugation. The proteins associate with the RNA C-rich motif as a 1:1:1 complex. The monomeric form of nsp1β within the complex differs from previously reported homodimer identified by X-ray crystallography. Functional analysis of the complex via mutational analysis combined with RNA-binding assays and cell-based frameshifting reporter assays reveal a number of key residues within nsp1β and PCBP2 that are involved in complex formation and function. Our results suggest that nsp1β and PCBP2 both interact directly with viral RNA during formation of the complex to coordinate this unusual PRF mechanism.

14 July 2020

18 August 2020

2 September 2020

Poly(ADP-ribose) polymerase (PARP) superfamily members covalently link either a single ADP-ribose (ADPR) or a chain of ADPR units to proteins using NAD as the source of ADPR. Although the well-known poly(ADP-ribosylating) (PARylating) PARPs primarily function in the DNA damage response, many noncanonical mono(ADP-ribosylating) (MARylating) PARPs are associated with cellular antiviral responses. We recently demonstrated robust up-regulation of several PARPs following infection with murine hepatitis virus (MHV), a model coronavirus. Here we show that SARS-CoV-2 infection strikingly up-regulates MARylating PARPs and induces the expression of genes encoding enzymes for salvage NAD synthesis from nicotinamide (NAM) and nicotinamide riboside (NR), while down-regulating other NAD biosynthetic pathways. We show that overexpression of PARP10 is sufficient to depress cellular NAD and that the activities of the transcriptionally induced enzymes PARP7, PARP10, PARP12 and PARP14 are limited by cellular NAD and can be enhanced by pharmacological activation of NAD synthesis. We further demonstrate that infection with MHV induces a severe attack on host cell NAD+ and NADP+. Finally, we show that NAMPT activation, NAM, and NR dramatically decrease the replication of an MHV that is sensitive to PARP activity. These data suggest that the antiviral activities of noncanonical PARP isozyme activities are limited by the availability of NAD and that nutritional and pharmacological interventions to enhance NAD levels may boost innate immunity to coronaviruses.

Climate migration: Ways ahead from the next generation The World Today rsoppelsa.drupal 25 May 2022

Ella Dennis and Mike Higgins talk to young activists seeking solutions as global warming wreaks havoc in sub-Saharan Africa

Africa has the lowest carbon emissions per capita yet the highest rate of temperature increase in the world. Rising levels of desertification, drought and flooding are already forcing millions of Africans to relocate to find more stable livelihoods. 

The continent’s youth will bear the brunt of this climate migration problem. It is estimated that by 2050, Africa will be home to 86 million internal climate migrants.

How is climate migration already affecting sub-Saharan Africa and what frameworks could tackle it? To begin to answer those questions, five young activists from across the region, who are members of Chatham House’s Common Futures Conversations, took part in a panel discussion at the world’s first youth-led Conference on Climate Migration, convened in April by the Alliance for Citizen Engagement, a nonpartisan think tank based in the US. 

The conversation and follow-up discussions focused on a common problem – climate migration brings people into conflict and puts pressure on infrastructure. 

In Kenya, droughts have left 3.5 million people hungry and the chronic flooding of several lakes in the Rift Valley has displaced hundreds of thousands, said Gerald Muchiri, 29, a social scientist from Kenya. One result has been outbreaks of violence between pastoralists such as the Orma people and the farmers of the Pokomo community, said Laura Mukhwana, 33, a PhD student in Kenya. She believes this violence is likely to worsen. ‘Inter-group conflicts will pose even larger security concerns for surrounding communities as climate migration intensifies,’ she said.

Suleman Nuhu, 24, a farmer and veterinary student from Nigeria, said farmer-herder conflicts were his country’s most significant climate-migration issue. The movement of nomadic tribes from the north had affected him personally: ‘Nomads have trespassed on [my family’s] farms many times while moving with their livestock, destroying our crops.’ 

Changes in climate also force people to move from rural to urban areas. Nigeria, for instance, struggles with the so-called ‘Lagos problem’, said Temiloluwa Lawal, 25, a lawyer and researcher from Nigeria. An estimated 22 million people, a number that is rising fast, are crammed into a city smaller than Greater London. While not on the same scale, Zimbabwe experiences comparable challenges, said Tinotenda Dube, 29, a Zimbabwean finance director. Thanks to drought, unemployed rural migrants arriving in cities ‘put excessive pressure on service delivery against a low tax base,’ he said. ‘People, including close family members of mine, are crowded in dilapidated homes because they cannot afford to pay rent for decent housing.’ 

But there is hope, say the activists. Dube believes that affordable housing is an ‘integral component of [tackling] the climate migration crisis’. 

In Zimbabwe, he has developed a low-cost home finance model that, he said, has helped more than 250 low-income households find good-quality accommodation. Alongside this initiative, Dube has co-founded a property and construction company, Solinfra Zimbabwe Private Ltd, to provide low-cost housing. 

Muchiri is taking action in Kenya, founding an NGO called Social Assistance Welfare to tackle public health issues, he said: ‘As climate migration becomes more intense, I expect preventable health issues to increase throughout the region, and thus see Social Assistance Welfare as an important mitigation.’

In Nigeria, Nuhu noted that to help reduce conflict between farmers and herders social-media campaigns are encouraging pastoralists to move from nomadic livestock farming to more efficient intensive systems, using ranching and grazing reserves. ‘As for food security problems, the best mitigation is to reduce reliance on rain-fed agriculture through irrigation schemes,’ he said. 

All five agreed that, in their experience, the youth of sub-Saharan Africa could be better informed about climate migration. But they took encouragement from the fact the young are passionate about tackling issues arising from the broader climate crisis. 

In Kenya, Mukhwana pointed to successful youth projects around agro-forestry and tree-planting. She added that there is ‘a growing movement of urban youth who are advocating for climate justice, such as the Kenyan Youth Environmental Network and Fridays for the Future Kenya’. It was pleasing too, she said, that when the Kenyan government revised its contributions to the Paris Climate Accords it staged a week-long youth conference to include their opinions.

‘Overall, I am quite hopeful about how the youth are mobilizing themselves in Kenya,’ she added.

Find out more about Chatham House’s Common Futures Conversations
 

The Climate Briefing: The nexus of water security and climate policy Audio NCapeling 22 August 2022

Examining the crossover between water security and climate change with the next two COPs taking place in regions with a history of being water stressed.

What should policymakers and negotiators from the Middle East and Africa working on water security focus on at COP27?

What does it mean to achieve water security? What are the main barriers or challenges? How is water security relevant to climate change?

This podcast was produced in collaboration with the UK Aid-funded Knowledge, Evidence and Learning for Development (K4D) programme which facilitates the use of evidence and learning in international development policy and programming.

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Last month, Sophos X-Ops reported several MDR cases where threat actors exploited a vulnerability in Veeam backup servers. We continue to track the activities of this threat cluster, which recently included deployment of a new ransomware. The vulnerability, CVE-2024-40711, was used as part of a threat activity cluster we named STAC 5881. Attacks leveraged compromised […]