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How genes affect tissue scale organization remains a longstanding biologicalpuzzle. As experimental efforts are underway to solve this puzzle viaquantification of gene expression and sub-cellular, cellular and tissuestructure, computational efforts remain far behind. To potentially helpaccelerate the computational efforts, we review two recent publications, thefirst on a cellular-based model for tissues and the second on a cell nucleusmodel consisting of chromatin and a lamina shell. We then give a perspective onhow the two models can be combined to test multiscale hypotheses linking thechromatin scale and the tissue scale. To be concrete, we turn to an in vitrosystem for the brain known as a brain organoid. We provide a multiscalehypothesis to distinguish structural differences between brain organoids builtfrom induced-pluripotent human stem cells and from induced-pluripotent gorillaand chimpanzee stem cells. Recent experiments discover that a cell fatetransition from neuroepithelial cells to radial glial cells includes a newintermediate state that is delayed in human-derived brain organoids as comparedto their genetically-close relatives, which significantly narrows and lengthensthe cells on the apical side [1]. Additional experiments revealed that theprotein ZEB2 plays a major role in the emergence of this new intermediate statewith ZEB2 mRNA levels peaking at the onset of the emergence [1]. We postulatethat the enhancement of ZEB2 expression driving this intermediate state ispotentially due to chromatin reorganization. More precisely, there existscritical strain triggering the reorganization that is higher for human-derivedstem cells, thereby resulting in a delay. Such a hypothesis can readily betested experimentally within individual cells and within brain organoids aswell as computationally to work towards solving the gene-to-tissue organizationpuzzle.

How human-derived brain organoids are built differently from brain organoids derived of genetically-close relatives: A multi-scale hypothesis