Q.59 Consider the following four experimental observations (i, ii, iii, iv) on the effect of the FT gene on flowering transition in the shoot apical meristem (SAM) of Arabidopsis thaliana. i) The FT promoter is active in leaves alone. ii) The ft null mutation causes delayed flowering transition of the SAM. iii) Expressing a recombinant FT protein fused to nuclear localization signal sequence under the endogenous promoter does not rescue the delayed-flowering phenotype of the ft null mutant. iv) Downregulation of FT transcript in the SAM by RNA interference in the wild-type background does not alter flowering transition. Which one of the following conclusions best explains the above observations? (A) FT protein resident in leaves causes flowering transition of the SAM. (B) FT transcript moves from leaves to the meristem and promotes flowering. (C) FT protein moves from leaves to the SAM and promotes flowering. (D) Both FT transcript and FT protein are required in the SAM to promote flowering.

Q.59 Consider the following four experimental observations (i, ii, iii, iv) on the effect of
the FT gene on flowering transition in the shoot apical meristem (SAM) of
Arabidopsis thaliana.

i)
The FT promoter is active in leaves alone.
ii) The
ft null mutation causes delayed flowering transition of the SAM.
iii)
Expressing a recombinant FT protein fused to nuclear localization signal
sequence under the endogenous promoter does not rescue the delayedflowering
phenotype of the ft null mutant.

iv)
Downregulation of FT transcript in the SAM by RNA interference in the
wildtype background does not alter flowering transition.

Which one of the following conclusions best explains the above observations?

(A)
FT protein resident in leaves causes flowering transition of the SAM.
(B)
FT transcript moves from leaves to the meristem and promotes flowering.
(C)
FT protein moves from leaves to the SAM and promotes flowering.
(D)
Both FT transcript and FT protein are required in the SAM to promote flowering.

FT protein moves from leaves to the shoot apical meristem (SAM) in Arabidopsis thaliana to promote flowering transition.

This mechanism explains the four observations on the FT gene’s role in flowering.

Observation Analysis

The FT promoter activates exclusively in leaf tissues, not the SAM. Null ft mutations delay SAM flowering transition due to absent FT signal from leaves. Nuclear-localized recombinant FT under the endogenous promoter fails to rescue ft mutants because it traps FT in leaf nuclei, blocking phloem transport to SAM. RNA interference targeting FT transcripts in wild-type SAM does not affect flowering, confirming no local FT transcription or transcript requirement there.

Option Evaluation

Option A fails because FT resident solely in leaves cannot signal distant SAM without mobility.

Option B is incorrect as FT transcripts show limited or no essential long-distance mobility for flowering; protein transport dominates.

Option C is correct since FT protein synthesized in leaves travels via phloem to interact with FD in SAM, activating floral genes like AP1 and LFY.

Option D is wrong because neither FT transcript nor protein needs local SAM production; leaf-derived protein suffices.

Introduction: Decoding FT Gene Role in Flowering

In Arabidopsis thaliana, the FT gene orchestrates flowering transition in the shoot apical meristem (SAM) through precise signaling from leaves. Experimental observations reveal FT promoter activity confined to leaves, ft null mutation delaying SAM transition, failed rescue by nuclear-localized FT, and no effect from SAM-specific FT knockdown. These pinpoint FT protein movement from leaves to SAM as the core mechanism.

FT Promoter and Expression Pattern

FT promoter drives expression solely in leaf phloem companion cells under long-day conditions, ensuring no direct SAM transcription. This leaf-specificity positions FT as a systemic signal, or florigen, synthesized away from its action site. Wild-type plants rely on this pattern for timely flowering.

Impact of ft Null Mutation

ft null mutants exhibit delayed flowering with excess vegetative leaves, as no FT reaches SAM to activate floral identity genes like APETALA1 (AP1) and LEAFY (LFY). Genetic studies confirm FT’s necessity for photoperiodic flowering promotion.

Nuclear Localization Signal Experiment

Recombinant FT fused to a nuclear localization signal (NLS), expressed under the endogenous leaf promoter, sequesters protein in leaf nuclei. This prevents phloem loading and transport to SAM, failing to rescue delayed flowering in ft null backgrounds. The result proves mobile, non-nuclear FT protein—not trapped or locally made—is essential.

SAM RNA Interference Findings

Downregulating FT transcripts via RNAi in wild-type SAM leaves flowering unchanged, indicating negligible endogenous FT expression or transcript function there. Leaf-derived protein alone suffices, ruling out local requirements.

Correct Conclusion: Protein Mobility Model

FT protein, not transcript, travels from leaf veins through phloem to SAM, forming an FT-FD complex that induces floral meristem identity. This aligns all observations and excludes alternatives. For CSIR NET aspirants, master this: FT exemplifies proteinaceous florigen in plant developmental biology.

Leave a Reply

Your email address will not be published. Required fields are marked *

Latest Courses