Informality, Gender Employment Gap, and COVID-19 in Mexico: Identifying Persistence and Dynamic Structural Effects

The objective is to analyze the impact of the COVID-19 pandemic on the dynamics of the Mexican labor market (formal-informal employment) by gender. It is built consistent micro-founded time-series from 1987:Q1 to 2019:Q4 using the Mexican urban employment surveys and estimate a VAR model linking aggregate production and each market segment. Our results suggest significant adverse effects on formal employment resulting from the COVID-19 pandemic, with lengthy job recovery for females and males. The informal sector in both genders presents a lower forecasted response to the initial production shock but substantial observed employment losses, potentially linked to structural changes in the market. In the COVID-19 crisis, the informal sector is not a substitute for formal employment losses. The complexity of this crisis suggests crafting policies to improve the easiness of the market to enhance formal job recovery while promoting gender equality. Our main contribution is to estimate the diverse employment losses by segments and a critical structural change in the labor market dynamics resulting from the COVID-19 pandemic focusing on urban employment.Informalidad, brecha de género en el empleo y COVID-19 en México: identificando la persistencia y los efectos estructurales dinámicosEl objetivo es analizar el impacto de la pandemia del COVID-19 en la dinámica del mercado laboral mexicano (empleo formal-informal) por género. Se construyen series de tiempo microfundamentales consistentes desde 1987:Q1 hasta 2019:Q4 utilizando las encuestas de empleo urbanas mexicanas, y se estima un modelo VAR que vincula la producción agregada y cada segmento del mercado. Nuestros resultados sugieren que hay efectos adversos significativos en el empleo formal como resultado de la pandemia del COVID-19, con una larga recuperación del empleo para las mujeres y los hombres. El sector informal, en ambos sexos, presenta una respuesta pronosticada menor al choque de producción inicial, pero pérdidas sustanciales de empleo observadas, potencialmente vinculadas a cambios estructurales en el mercado. En la crisis de COVID-19, el sector informal no es un sustituto de las pérdidas de empleo formal. La complejidad de esta crisis sugiere la elaboración de políticas que mejoren la facilidad del mercado para potenciar la recuperación del empleo formal al tiempo que se promueve la igualdad de género. Nuestra principal contribución es estimar las diversas pérdidas de empleo por segmentos y un cambio estructural crítico en la dinámica del mercado laboral resultante de la pandemia de COVID-19, centrando el análisis en el empleo urbano

Rare and low-frequency coding variants alter human adult height

Height is a highly heritable, classic polygenic trait with ~700 common associated variants identified so far through genome - wide association studies . Here , we report 83 height - associated coding variants with lower minor allele frequenc ies ( range of 0.1 - 4.8% ) and effects of up to 2 16 cm /allele ( e.g. in IHH , STC2 , AR and CRISPLD2 ) , >10 times the average effect of common variants . In functional follow - up studies, rare height - increasing alleles of STC2 (+1 - 2 cm/allele) compromise d proteolytic inhibition of PAPP - A and increased cleavage of IGFBP - 4 in vitro , resulting in higher bioavailability of insulin - like growth factors . The se 83 height - associated variants overlap genes mutated in monogenic growth disorders and highlight new biological candidates ( e.g. ADAMTS3, IL11RA, NOX4 ) and pathways ( e.g . proteoglycan/ glycosaminoglycan synthesis ) involved in growth . Our results demonstrate that sufficiently large sample sizes can uncover rare and low - frequency variants of moderate to large effect associated with polygenic human phenotypes , and that these variants implicate relevant genes and pathways

Employment, wages, and the gender gap in Mexico: Evidence of three decades of the urban labor market

El objetivo de este artículo es analizar la evidencia histórica de la brecha de género en el empleo y los salarios en México. Para ello, construimos series de tiempo consistentes desde 1988:Q1 hasta 2019:Q4 utilizando encuestas de empleo en México, y estimamos en cada trimestre un modelo de participación laboral y salarios para cada segmento de género del mercado formal, corrigiendo el sesgo de selección correspondiente. A partir de estos resultados, implementamos una descomposición Blinder-Oaxaca (1973) y Mulligan-Rubinstein (2008) para estimar la brecha salarial de género. Nuestros resultados sugieren que los rendimientos de la escolaridad para ambos géneros han disminuido en las dos últimas décadas, mostrando una brecha de casi 2% a favor de las mujeres. La diferencia salarial entre ambos sexos fluctúa en torno al 29.6% una vez corregido el sesgo de autoselección. La prevalencia de las diferencias en los salarios esperados entre géneros existe debido a los efectos de "sesgo de selección" y "residual". Una limitación de este trabajo es que sólo se centra en el empleo urbano formal en 16 áreas metropolitanas; sin embargo, este enfoque permite identificar las tendencias de largo plazo y los cambios estructurales en este mercado, expandiendo la evidencia de la brecha de género en la historia económica mexicana

Genome-wide association study identifies 48 common genetic variants associated with handedness.

Handedness has been extensively studied because of its relationship with language and the over-representation of left-handers in some neurodevelopmental disorders. Using data from the UK Biobank, 23andMe and the International Handedness Consortium, we conducted a genome-wide association meta-analysis of handedness (N = 1,766,671). We found 41 loci associated (P < 5 × 10-8) with left-handedness and 7 associated with ambidexterity. Tissue-enrichment analysis implicated the CNS in the aetiology of handedness. Pathways including regulation of microtubules and brain morphology were also highlighted. We found suggestive positive genetic correlations between left-handedness and neuropsychiatric traits, including schizophrenia and bipolar disorder. Furthermore, the genetic correlation between left-handedness and ambidexterity is low (rG = 0.26), which implies that these traits are largely influenced by different genetic mechanisms. Our findings suggest that handedness is highly polygenic and that the genetic variants that predispose to left-handedness may underlie part of the association with some psychiatric disorders

Rare and low-frequency coding variants alter human adult height

Height is a highly heritable, classic polygenic trait with approximately 700 common associated variants identified through genome-wide association studies so far. Here, we report 83 height-associated coding variants with lower minor-allele frequencies (in the range of 0.1-4.8%) and effects of up to 2 centimetres per allele (such as those in IHH, STC2, AR and CRISPLD2), greater than ten times the average effect of common variants. In functional follow-up studies, rare height-increasing alleles of STC2 (giving an increase of 1-2 centimetres per allele) compromised proteolytic inhibition of PAPP-A and increased cleavage of

A saturated map of common genetic variants associated with human height

Common single-nucleotide polymorphisms (SNPs) are predicted to collectively explain 40-50% of phenotypic variation in human height, but identifying the specific variants and associated regions requires huge sample sizes. Here, using data from a genome-wide association study of 5.4 million individuals of diverse ancestries, we show that 12,111 independent SNPs that are significantly associated with height account for nearly all of the common SNP-based heritability. These SNPs are clustered within 7,209 non-overlapping genomic segments with a mean size of around 90 kb, covering about 21% of the genome. The density of independent associations varies across the genome and the regions of increased density are enriched for biologically relevant genes. In out-of-sample estimation and prediction, the 12,111 SNPs (or all SNPs in the HapMap 3 panel) account for 40% (45%) of phenotypic variance in populations of European ancestry but only around 10-20% (14-24%) in populations of other ancestries. Effect sizes, associated regions and gene prioritization are similar across ancestries, indicating that reduced prediction accuracy is likely to be explained by linkage disequilibrium and differences in allele frequency within associated regions. Finally, we show that the relevant biological pathways are detectable with smaller sample sizes than are needed to implicate causal genes and variants. Overall, this study provides a comprehensive map of specific genomic regions that contain the vast majority of common height-associated variants. Although this map is saturated for populations of European ancestry, further research is needed to achieve equivalent saturation in other ancestries

A saturated map of common genetic variants associated with human height

Common single-nucleotide polymorphisms (SNPs) are predicted to collectively explain 40–50% of phenotypic variation in human height, but identifying the specific variants and associated regions requires huge sample sizes1. Here, using data from a genome-wide association study of 5.4 million individuals of diverse ancestries, we show that 12,111 independent SNPs that are significantly associated with height account for nearly all of the common SNP-based heritability. These SNPs are clustered within 7,209 non-overlapping genomic segments with a mean size of around 90 kb, covering about 21% of the genome. The density of independent associations varies across the genome and the regions of increased density are enriched for biologically relevant genes. In out-of-sample estimation and prediction, the 12,111 SNPs (or all SNPs in the HapMap 3 panel2) account for 40% (45%) of phenotypic variance in populations of European ancestry but only around 10–20% (14–24%) in populations of other ancestries. Effect sizes, associated regions and gene prioritization are similar across ancestries, indicating that reduced prediction accuracy is likely to be explained by linkage disequilibrium and differences in allele frequency within associated regions. Finally, we show that the relevant biological pathways are detectable with smaller sample sizes than are needed to implicate causal genes and variants. Overall, this study provides a comprehensive map of specific genomic regions that contain the vast majority of common height-associated variants. Although this map is saturated for populations of European ancestry, further research is needed to achieve equivalent saturation in other ancestries

Publisher Correction: Protein-altering variants associated with body mass index implicate pathways that control energy intake and expenditure in obesity

In the HTML version of this article initially published, the author groups ‘CHD Exome+ Consortium’, ‘EPIC-CVD Consortium’, ‘ExomeBP Consortium’, ‘Global Lipids Genetic Consortium’, ‘GoT2D Genes Consortium’, ‘EPIC InterAct Consortium’, ‘INTERVAL Study’, ‘ReproGen Consortium’, ‘T2D-Genes Consortium’, ‘The MAGIC Investigators’ and ‘Understanding Society Scientific Group’ appeared at the end of the author list but should have appeared earlier in the list, after author Krina T. Zondervan. The errors have been corrected in the HTML version of the article

Protein-altering variants associated with body mass index implicate pathways that control energy intake and expenditure in obesity

Genome-wide association studies (GWAS) have identified >250 loci for body mass index (BMI), implicating pathways related to neuronal biology. Most GWAS loci represent clusters of common, noncoding variants from which pinpointing causal genes remains challenging. Here we combined data from 718,734 individuals to discover rare and low-frequency (minor allele frequency (MAF) < 5%) coding variants associated with BMI. We identified 14 coding variants in 13 genes, of which 8 variants were in genes (ZBTB7B, ACHE, RAPGEF3, RAB21, ZFHX3, ENTPD6, ZFR2 and ZNF169) newly implicated in human obesity, 2 variants were in genes (MC4R and KSR2) previously observed to be mutated in extreme obesity and 2 variants were in GIPR. The effect sizes of rare variants are ~10 times larger than those of common variants, with the largest effect observed in carriers of an MC4R mutation introducing a stop codon (p.Tyr35Ter, MAF = 0.01%), who weighed ~7 kg more than non-carriers. Pathway analyses based on the variants associated with BMI confirm enrichment of neuronal genes and provide new evidence for adipocyte and energy expenditure biology, widening the potential of genetically supported therapeutic targets in obesity