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Biology subjects

Gilani, H.

Publications and source records attributed to Gilani, H..

2 recordsLinked to original sources

The global spectrum of tree crown architecture

Trees can differ enormously in their crown architectural traits, such as the scaling relationships that link their height and crown size to their stem diameter. Yet despite the importance of crown architecture in shaping the structure and function of woody ecosystems, we lack a complete picture of what drives this incredible diversity in crown shapes. Using data from >500,000 globally distributed trees, we explored how climate, disturbance, competition, functional traits, and evolutionary history constrain the height, crown size and shape of the worlds tree species. We found that variation in height scaling relationships was primarily controlled by water availability and light competition. Conversely, crown width was predominantly shaped by exposure to wind and fire, while also covarying with other functional traits related to mechanical stability and photosynthesis. Additionally, several plant lineages had crown architectures that defy their environments, such as the exceedingly slender dipterocarps of Southeast Asia, or the extremely wide crowns of legumes in African savannas. Our study charts the global spectrum of tree crown architectural types. It provides a roadmap for integrating crown architecture with vegetation models and remote sensing observations, so that we may better understand the processes that shape the 3D structure of woody ecosystems.

ecology↗

Genetic regulation of human aortic smooth muscle cell gene expression and splicing predict causal coronary artery disease genes

Coronary artery disease (CAD) is the leading cause of death worldwide. Recent meta-analyses of genome-wide association studies (GWAS) have identified over 175 loci associated with CAD. The majority of these loci are in non-coding regions and are predicted to regulate gene expression. Given that vascular smooth muscle cells (SMCs) play critical roles in the development and progression of CAD, we hypothesized that a subset of the CAD GWAS risk loci are associated with the regulation of transcription in distinct SMC phenotypes. Here, we measured gene expression in SMCs isolated from the ascending aortas of 151 ethnically diverse heart transplant donors in quiescent or proliferative conditions and calculated the association of their expression and splicing with [~]6.3 million imputed single nucleotide polymorphism (SNP) markers across the genome. We identified 4,910 expression and 4,412 splice quantitative trait loci (sQTL) that represent regions of the genome associated with transcript abundance and splicing. 3,660 of the eQTLs had not been observed in the publicly available Genotype-Tissue Expression dataset. Further, 29 and 880 of the eQTLs were SMC- and sex-specific, respectively. To identify the effector transcript(s) regulated by CAD GWAS loci, we used four distinct colocalization approaches and identified 84 eQTL and 164 sQTLs that colocalized with CAD loci, highlighting the importance of genetic regulation of mRNA splicing as a molecular mechanism for CAD genetic risk. Notably, 20% and 35% of the eQTLs were unique to quiescent or proliferative SMCs, respectively. Two CAD loci colocalized with a SMC sex-specific eQTL (AL160313.1 and TERF2IP) and another locus colocalized with SMC-specific eQTL (ALKBH8). Also, 27% and 37% of the sQTLs were unique to quiescent or proliferative SMCs, respectively. The most significantly associated CAD locus, 9p21, was an sQTL for the long non-coding RNA CDKN2B-AS1, also known as ANRIL, in proliferative SMCs. Collectively, these results provide evidence for the molecular mechanisms of genetic susceptibility to CAD in distinct SMC phenotypes.

genetics↗