Thylakoid membrane transporter SecE1 is required for chloroplast development and photosynthetic function in Arabidopsis.

Chloroplast biogenesis depends on protein transport, pigment biosynthesis, and thylakoid membrane assembly, which are coordinated through anterograde (nucleus-to-plastid) and retrograde (plastid-to-nucleus) signaling. The chloroplast Sec translocon mediates the import of nuclear-encoded precursor proteins across the thylakoid membrane, yet the regulatory role of its core subunit SecE1 in chloroplast development and photosynthetic performance remains incompletely understood. Here, we characterized a chlorotic Arabidopsis mutant with partial loss of SecE1 function. Compared with the wild type and a complementation lin, the sece1 exhibited retarded leaf growth, reduced chlorophyll accumulation, and diminished maximum photochemical efficiency (Fv/Fm), indicative of impaired photosynthetic competence. Biochemical analyses further revealed compromised assembly and stability of photosynthetic supercomplexes, along with decreased abundance of Sec1 transporter substrates and key PSII subunits. Notably, these plastid defects triggered extensive transcriptional reprogramming, marked by altered expression of genes functioning in retrograde signaling transduction, transcription factor activity, and nuclear-encoded photosynthetic regulators, a feature indicative of retrograde-triggered compensatory responses in the sece1. Collectively, our findings demonstrate that SecE1 is critically required for chloroplast biogenesis by sustaining photosynthetic protein transport and accumulation, as well as supercomplex assembly, and that its loss elicits retrograde signals that reshape nuclear gene expression to mitigate plastid dysfunction. This study highlights the interplay between thylakoid protein translocation and organellar-nuclear communication as a determinant of photosynthetic competence and plant growth.