YGL46 encoding ferredoxin-like protein interacts with FTR and CAO to regulate chlorophyll synthesis and leaf development in maize.
TL;DR
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, and interacts with chlorophyllide a oxygenase (ZmCAO, Zm00001d002408) to regulate chlorophyll b (Chl b) biosynthesis.
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.