rs11545787 — RASD1 RASD1 photic entrainment variant

3' UTR variant in RASD1 (Dexras1), a GTPase that gates light signals to the circadian clock in the suprachiasmatic nucleus; the G allele is associated with earlier chronotype (morningness)

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RASD1 — The Molecular Gatekeeper of Your Light-Clock Connection

Every morning, light entering your eyes triggers a cascade that resets your internal clock. At the center of this process — in the suprachiasmatic nucleus (SCN), the brain's master pacemaker — sits a small GTP-binding protein called Dexras1, encoded by the RASD1 gene. Dexras1 acts as a molecular gatekeeper: it decides how strongly a light signal translates into a shift of the circadian clock. The rs11545787 variant in the RASD1 gene's 3' UTR region influences this gating function, and in a genome-wide study of nearly 90,000 people, it emerged as one of only 15 loci that significantly predict whether a person identifies as a morning or evening type.

The Mechanism

Dexras1 is a Ras-superfamily small GTPase11 Ras-superfamily small GTPase
A molecular switch protein that cycles between active GTP-bound and inactive GDP-bound states, coupling upstream signals to downstream effectors expressed in a circadian pattern in the SCN, with peak levels during subjective night — precisely when the clock is most sensitive to light. When photons arrive in the early night (triggering phase delays) or late night (triggering phase advances), retinal ganglion cells relay signals via the retinohypothalamic tract to SCN neurons, activating NMDA receptors22 NMDA receptors
N-methyl-D-aspartate receptors — glutamate-gated ion channels that open in response to synaptic input from the retina, allowing calcium influx that activates downstream signaling.

Calcium influx activates nitric oxide synthase, which produces nitric oxide that S-nitrosylates Dexras1, switching it to its active GTP-bound form. Active Dexras1 then couples to Gi/o proteins and the ERK/MAPK signaling cascade33 Active Dexras1 then couples to Gi/o proteins and the ERK/MAPK signaling cascade
Cheng et al. 2004 Neuron: Dexras1 potentiates photic and suppresses nonphotic responses of the circadian clock, amplifying the light signal's ability to shift the molecular clock. During the late night, Dexras1 additionally suppresses the PACAP/PAC1 pathway, sculpting the phase response curve so the clock responds appropriately at each time of day rather than indiscriminately to any light exposure.

Mice lacking Dexras144 Mice lacking Dexras1
Cheng et al. 2006 Journal of Neuroscience show reduced photic phase shifts in the early night (when Dexras1 normally amplifies light signals via NMDA-ERK coupling) and paradoxical phase shifts during daytime (when Dexras1 normally gates out light). The rs11545787 variant sits in the 3' UTR — a region that regulates mRNA stability and translation efficiency — and likely modulates RASD1 expression level, with the G allele correlating with slightly enhanced entrainment to morning light.

The Evidence

The G allele association with morningness was first identified in Hu et al. 2016 (Nature Communications)55 Hu et al. 2016 (Nature Communications)
GWAS of 89,283 individuals identifying 15 morningness loci including rs11545787 near RASD1 at P=1.4×10⁻⁸, a landmark 23andMe GWAS covering 89,283 individuals. The RASD1 locus was one of only seven identified near established circadian genes (alongside RGS16, VIP, PER2, HCRTR2, PER3, and FBXL3), placing it in select company.

The finding was substantially replicated and strengthened in Jones et al. 2019 (Nature Communications)66 Jones et al. 2019 (Nature Communications)
GWAS of 697,828 individuals expanding chronotype loci to 351 and confirming the RASD1 locus with OR ~1.05 per G allele, P=4×10⁻³⁰, a mega-GWAS of 697,828 UK Biobank and 23andMe participants that expanded the total morningness loci from 24 to 351. The RASD1 locus remained significant (P=4×10⁻³⁰, OR ~1.05 per G allele), confirmed as a genuine chronotype signal. Each G allele is associated with approximately a 3–5 minute earlier average wake time, with the extremes — top 5% vs. bottom 5% of polygenic morningness scores — differing by 25 minutes in sleep timing across all variants combined.

Mechanistic support comes from animal studies: Dexras1-null mice77 Dexras1-null mice
Cheng et al. 2004 Neuron entrain poorly to dim light cycles and show blunted phase-shifting to light pulses. Rhythmic RASD1 expression in the SCN88 Rhythmic RASD1 expression in the SCN
Takahashi et al. 2003 Brain Research Mol Brain Research with ~fivefold amplitude peaks at subjective night supports the gene's functional relevance to photic gating.

Practical Actions

People with the AA genotype have fewer G (morningness) alleles, which is associated with a slight evening chronotype tendency. This does not mean they have a disorder — it means their light-entrainment pathway is slightly less amplified in the morning-light direction. The most effective personalized strategy is optimizing the timing and intensity of morning light exposure to compensate for the reduced photic gating signal, and protecting the evening environment from artificial light that could further delay the clock. AG carriers occupy the intermediate range. GG carriers have the strongest biological pull toward morningness but can still be disrupted by late-night light or irregular schedules.

For jet lag and shift work, RASD1 genotype is relevant to how quickly the clock resets: individuals with stronger photic sensitivity (GG) may recover more readily from eastward travel (which requires phase advances) via bright morning light, while AA individuals may need more consistent bright-light timing to achieve equivalent shifts.

Interactions

RASD1 sits downstream of the retinohypothalamic tract and feeds into the same ERK/MAPK and core clock loop as PER2 (rs35333999), PER3 (rs228697, rs10462020), CRY1 (rs2287161), and CLOCK (rs1801260). A person carrying eveningness alleles at multiple loci — e.g., an AA genotype here combined with variants reducing PER3 or CLOCK function — would have a compounded evening chronotype phenotype, and may find that social demands (early work schedules, school start times) create chronic circadian misalignment. The aggregate effect of morningness alleles across all 351 loci spans ~25 minutes of sleep timing, meaning no single variant dominates — polygenic context matters.

Genotype Interpretations

What each possible genotype means for this variant.

GG Morning-Type Normal

Strong biological pull toward morningness

The GG genotype is associated with the highest photic gating activity via Dexras1 in the SCN. In population terms, GG individuals self-report morning preference at the highest rate among the three genotype groups. This aligns with the GWAS finding (OR ~1.05 per G allele for morningness across 697,828 participants). Your circadian clock resets efficiently in response to morning bright light, which supports stable early entrainment — an advantage for conventional work schedules and early-morning activities.

AG Intermediate Chronotype Intermediate

Mild evening tendency — morning light timing matters

Heterozygous AG carriers have one copy each of the morningness (G) and the weaker-photic-gating (A) allele. The additive effect means intermediate Dexras1 expression or function in the SCN — your clock still responds well to light but with slightly less amplitude than GG. In practice this manifests as greater variability in preferred wake time, and higher susceptibility to schedule drift when morning light is inconsistent (e.g., winter months, indoor work, travel). Targeted bright-light timing in the morning can reliably anchor your clock despite the A allele's modest attenuating effect.

AA Evening-Type Decreased

Evening chronotype tendency — photic entrainment is less amplified

The AA genotype is associated with the strongest evening-type tendency via the RASD1 locus. With both G alleles absent, Dexras1-mediated amplification of photic signals in the early morning is at its lowest, meaning your clock needs more intense or more consistently timed light to achieve equivalent entrainment compared to GG individuals. Left unconstrained, AA individuals tend toward later natural bedtimes and wake times. The gap between biological sleep timing and work/school schedules constitutes social jet lag — a form of chronic circadian misalignment linked to mood instability, metabolic changes, and reduced cognitive performance during morning hours.

The RASD1 locus alone contributes only a small fraction of chronotype variance — polygenic context matters greatly. AA at rs11545787 combined with evening-type alleles at PER2 (rs35333999), PER3 (rs228697, rs10462020), CRY1 (rs2287161), or CLOCK (rs1801260) would compound the evening tendency.