Loss of the plant DEAD-box protein ISE1 leads to defective mitochondria and increased cell-to-cell transport via plasmodesmata.

Abstract:

:Plants have intercellular channels, plasmodesmata (PD), that span the cell wall to enable cell-to-cell transport of micro- and macromolecules. We identified an Arabidopsis thaliana embryo lethal mutant increased size exclusion limit 1 (ise1) that results in increased PD-mediated transport of fluorescent tracers. The ise1 mutants have a higher frequency of branched and twinned PD than wild-type embryos. Silencing of ISE1 in mature Nicotiana benthamiana leaves also leads to increased PD transport, as monitored by intercellular movement of a GFP fusion to the tobacco mosaic virus movement protein. ISE1 encodes a putative plant-specific DEAD-box RNA helicase that localizes specifically to mitochondria. The N-terminal 100 aa of ISE1 specify mitochondrial targeting. Mitochondrial metabolism is compromised severely in ise1 mutant embryos, because their mitochondrial proton gradient is disrupted and reactive oxygen species production is increased. Although mitochondria are essential for numerous cell-autonomous functions, the present studies demonstrate that mitochondrial function also regulates the critical cell non-cell-autonomous function of PD.

authors

Stonebloom S,Burch-Smith T,Kim I,Meinke D,Mindrinos M,Zambryski P

doi

10.1073/pnas.0909229106

subject

Has Abstract

pub_date

2009-10-06 00:00:00

pages

17229-34

issue

40

eissn

0027-8424

issn

1091-6490

pii

0909229106

journal_volume

106

pub_type

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