A new study, published today in the journal EMBO Reports* and conducted in the laboratory led by Paula Duque, researcher at the Gulbenkian Institute for Molecular Medicine (GIMM), reveals an unexpected function of a plant stress hormone: abscisic acid (ABA) prevents embryonic leaves called cotyledons from opening while still in darkness.
When a seed buried in the soil germinates, the young plant finds itself in a light-free environment with limited resources. To survive, it grows rapidly to reach the surface and needs to precisely control when it activates processes that prepare it for light exposure. A critical step in this transition is the opening of cotyledons – small embryonic leaves that, when opened, begin to capture solar energy and perform photosynthesis, marking the beginning of the plant’s autotrophic growth. The new study shows that, before light exposure, ABA accumulated in the cotyledons prevents their opening, preventing premature activation of this process.
“ABA is known for helping plants deal with stress situations, such as drought or high salinity,” explains Paula Duque. “But we have now discovered that it also has a key role in the normal development of the young plant, functioning as a molecular brake that prevents cotyledons from opening too early.”
This discovery was made through experiments on Arabidopsis thaliana, a model plant widely used in scientific research. The researchers analyzed not only the physiological effects of ABA on cotyledon opening but also the genetic and molecular mechanisms behind this unexpected hormone function. The study shows that ABA significantly interferes with how genes are read and processed during this critical stage of plant development.
More specifically, the hormone acts on a process called alternative splicing, a kind of genetic editing that defines how the information contained in DNA is transformed into proteins. This process allows plants to generate different versions of their proteins from the same genes, depending on environmental conditions. The study reveals that ABA modulates this process through two key proteins from the SR (serine and arginine-rich) protein family: RS40 and RS41.
These proteins act as splicing regulators and are essential for adjusting the plant’s gene expression patterns in response to light. The study shows that in darkness, ABA reduces the activity of these proteins, preventing the genetic changes necessary for cotyledon opening. Additionally, the authors identified an additional control mechanism: the repression exerted by ABA depends on phosphorylation processes – a chemical modification that regulates protein function.
“This discovery offers a new perspective on how plants integrate hormonal and environmental signals to control their development,” highlights Guiomar Martín, the study’s first author. “Besides being scientifically fascinating, it may have relevant practical implications, for example in creating crops with more efficient early development or greater resistance to adverse conditions.”
Although at first glance this process might seem like a technical detail of plant biology, understanding how the young plant adjusts its development to the surrounding environment is fundamental to optimizing agricultural crop growth and productivity. Regulating cotyledon opening has a direct impact on plant survival and vigor, especially in low-light environments or subject to unpredictable climates.
By revealing this new layer of genetic regulation mediated by ABA – an intersection point between hormonal, environmental, and molecular signals – the work highlights how seemingly simple processes can hide remarkable biological complexity. It also reinforces the importance of fundamental research in plant biology, whose knowledge can, in the medium term, inspire innovative strategies in sustainable agriculture, food security, and climate change adaptation.
Martín G, Confraria A, Zapata I, Larran AS, Qüesta J, Duque P (2025). Cotyledon opening during seedling deetiolation is determined by ABA-mediated splicing regulation. EMBO Reports. DOI: 10.1038/s44319-025-00495-5
This work was developed at GIMM – Gulbenkian Institute for Molecular Medicine, Portugal, in collaboration with the Centre for Research in Agricultural Genomics (CRAG), Barcelona, Spain.