Hexaploid triticale results from crosses between durum wheat and rye. Despite its high agronomic potential, triticale is mainly used for livestock feed. Triticale surpasses their parental species in adaptability and tolerance to abiotic and biotic stresses, being able to grow in acidic soils where a high amount of iron (Fe) and zinc (Zn) is typical. On the other hand, high amounts of these essential trace elements can be cytotoxic to bread wheat. The cytotoxicity induced by seed priming with a high concentration of Fe and Zn impaired root cell division and induced nucleolar changes in bread wheat. Such cytogenetic approaches were expedited and successfully determined cytotoxic and suited micronutrient dosages for wheat nutripriming. With this study, we intended to analyse the hexaploid triticale cv ‘Douro’ root mitotic cell cycle and nucleolar activity after seed priming performed with aqueous solutions of iron (Fe) and/or zinc (Zn), containing a concentration that was previously considered cytotoxic, to bread wheat and to infer the higher tolerance of triticale to these treatments. The overall cytogenetic data allowed us to conclude that the Fe + Zn treatment enhanced the root mitotic index (MI), mitosis regularity and nucleolar activity of ‘Douro’ relative to the control and the individual treatments performed with Fe or Zn alone. The Fe + Zn treatment might suit triticale biofortification through seed priming.

Accurate transition into mitosis driven by cyclin B1-CDK1 activity is essential to avoid chromosome segregation errors and preserve genome integrity. How this activity is spatially controlled to trigger mitotic onset remains unclear. Here, we show that chromosome condensation triggers an increase in nuclear envelope (NE) tension. This increased tension is required for translocation of cyclin B1 into the nucleus and dynein loading on nuclear pore complexes (NPCs), ensuring timely mitotic entry. Micromanipulation experiments further indicate this tension-dependent mechanism requires SUN proteins on the NE. Impairment of chromosome condensation leads to the nuclear accumulation of the G2 checkpoint kinase Wee1 and an inhibition of CDK1 activity, which result in a temporary delay in mitotic entry. This delay can be overridden by increasing tension on the NE, which accelerates the nuclear translocation of cyclin B1 and dynein loading. We propose that mitotic onset is controlled by a chromosome-dependent NE tension mechanism that enables robust spatiotemporal coupling between chromosome condensation and the NE structural changes required for an efficient mitosis.