YGL46 encoding ferredoxin-like protein interacts with FTR and CAO to regulate chlorophyll synthesis and leaf development in maize.

Abstract

Chlorophyll is crucial in photosynthesis, enabling plants to absorb light energy for photosynthesis. Here, we identified a yellow-green leaf mutant ygl46 derived from natural variation. Phenotypic characterization exhibited pale leaves. In the mutant, chlorophyll accumulation was significantly reduced, especially chlorophyll b. The mutated phenotype is governed by a single recessive gene. The mutation site was mapped to a 270-kb physical interval between the Indel markers ID0270 and ID0302 on chromosome 5 using an F2 mapping population. A gene (Zm00001d013534) encoding ferredoxin-like (FdC2) protein with varied expression pattern was identified as the candidate gene. The precursor protoporphyrin IX (Proto IX) accumulated to higher levels, while downstream intermediates including Mg-protoporphyrin IX (MgP IX) and protochlorophyllide (Pchlide) were significantly decreased. Functional analysis showed that YGL46 interacts with ferredoxin-thioredoxin reductase (ZmFTR, Zm00001d045366), potentially functioning as an electron donor, to affect MgP IX accumulation, thereby regulating leaf development. In addition, YGL46 interacts with chlorophyllide a oxygenase (ZmCAO, Zm00001d002408) to regulate chlorophyll b (Chl b) biosynthesis.