Nondestructive analysis of senescence in mesophyll cells by spectral resolution of protein synthesis-dependent pigment metabolism
Article first published online: 11 MAR 2008
© The Authors (2008). Journal compilation © New Phytologist (2008)
Volume 179, Issue 3, pages 663–674, August 2008
How to Cite
Gay, A., Thomas, H., Roca, M., James, C., Taylor, J., Rowland, J. and Ougham, H. (2008), Nondestructive analysis of senescence in mesophyll cells by spectral resolution of protein synthesis-dependent pigment metabolism. New Phytologist, 179: 663–674. doi: 10.1111/j.1469-8137.2008.02412.x
- Issue published online: 15 JUL 2008
- Article first published online: 11 MAR 2008
- Received: 16 November 2007Accepted: 15 January 2008
- multivariate analysis;
- Systems Biology
- • Over 6 d of dark-induced senescence, leaf segments of wild-type Lolium temulentum lost > 96% chlorophyll a + b; leaves from plants containing a staygreen mutation introgressed from Festuca pratensis, which has a lesion in the senescence-associated fragmentation of pigment-proteolipid complexes, retained over 43% of total chlorophyll over the same period.
- • Mutant segments preferentially retained thylakoid membrane proteins (exemplified by LHCP II) but lost other cellular proteins at the same rate as wild-type tissue. The protein synthesis inhibitor D-MDMP inhibited chlorophyll degradation and partially prevented protein loss in both genotypes, but tissues treated with the ineffective L-stereoisomer were indistinguishable from water controls.
- • Principal-components analysis of leaf reflectance spectra distinguished between genotypes, time points and D-MDMP treatments, showing the disruption of pigment metabolism during senescence brought about by the staygreen mutation, by inhibition of protein synthesis and by combinations of the two factors.
- • The build-up of oxidized, dephytylated and phaeo-derivatives of chl a during senescence of staygreen tissue was prevented by D-MDMP and associated with characteristic difference spectra when senescent mutant tissue was compared with wild-type or inhibitor-treated samples. The suitability of senescence as a subject for systems biology approaches is discussed.